Wednesday, February 12, 2025

** **ACUTE MI/STEMI** **: Activate the cath lab if the patient has chest pain?

Written by Willy Frick

I was reviewing our institutional PMcardio account which we are using to improve early identification of patients with electrocardiographically subtle OMI. 

I came across this ECG:

What do you think?






Even before we have clinical context, this ECG simply does not appear concerning for OMI, notwithstanding the machine's interpretation ** ** ACUTE MI / STEMI ** **

I sent this ECG to Dr. Smith with no clinical context, and he immediately replied "Fake." 

I suspect most blog readers did not struggle with this one. But in the world of STEMI, this is a challenging ECG to most.

Furthermore, how many clinicians are truly comfortable setting aside the machine interpretation and sticking with their gut that this ECG does not look ischemic. Fortunately, the physicians seeing the patient were using the Queen of Hearts PM Cardio AI ECG OMI Model, and she had absolutely no concerns.


When the Queen has some suspicion of OMI, she asks if the patient has ACS Symptoms.  She did not even need to ask in this case, because even if the patient presented with chest pain, she would call it NEGATIVE.

When I reviewed the chart, I learned that the patient had presented with syncope. The emergency physician does cautiously (correctly) note that the ECG meets STEMI criteria in V3 and V4, but goes on to document absence of ACS symptoms. The patient ruled out for MI with serial troponin testing.

Most impressively, cardiology was never consulted! This reassuring assistance from AI improved the patient's care by preventing unneeded additional testing and involvement of specialists.

The Queen of Hearts not only is extremely sensitive for subtle OMI, but is also great at recognizing false positive ECGs.

The Queen decreases false positive cath lab activations.

We published this study, showing that false positive prehospital cath lab activations would be decreased by 58% if they used the Queen:


Artificial Intelligence Driven Prehospital ECG Interpretation for the Reduction of False Positive Emergent Cardiac Catheterization Lab Activations: A Retrospective Cohort Study


Abstract

Objectives

Data suggest patients suffering acute coronary occlusion myocardial infarction (OMI) benefit from prompt primary percutaneous intervention (PPCI). Many emergency medical services (EMS) activate catheterization labs to reduce time to PPCI, but suffer a high burden of inappropriate activations. Artificial intelligence (AI) algorithms show promise to improve electrocardiogram (ECG) interpretation. The primary objective was to evaluate the potential of AI to reduce false positive activations without missing OMI.

Methods

Electrocardiograms were categorized by (1) STEMI criteria, (2) ECG integrated device software and (3) a proprietary AI algorithm (Queen of Hearts (QOH), Powerful Medical). If multiple ECGs were obtained and any one tracing was positive for a given method, that diagnostic method was considered positive. The primary outcome was OMI defined as an angiographic culprit lesion with either TIMI 0–2 flow; or TIMI 3 flow with either peak high sensitivity troponin-I > 5000 ng/L or new wall motion abnormality. The primary analysis was per-patient proportion of false positives.

Results

A total of 140 patients were screened and 117 met criteria. Of these, 48 met the primary outcome criteria of OMI. There were 80 positives by STEMI criteria, 88 by device algorithm, and 77 by AI software. All approaches reduced false positives, 27% for STEMI, 22% for device software, and 34% for AI (p < 0.01 for all). The reduction in false positives did not significantly differ between STEMI criteria and AI software (p = 0.19) but STEMI criteria missed 6 (5%) OMIs, while AI missed none (p = 0.01).

Conclusions

In this single-center retrospective study, an AI-driven algorithm reduced false positive diagnoses of OMI compared to EMS clinician gestalt. Compared to AI (which missed no OMI), STEMI criteria also reduced false positives but missed 6 true OMI. External validation of these findings in prospective cohorts is indicated.




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MY Comment, by KEN GRAUER, MD (2/12/2025):  
===================================
As per Dr. Frick — the ST elevation and T wave inversion in today's ECG is not the result of an acute OMI. Instead — it is almost certain to be a longstanding finding in this patient with marked LVH.
  • As I emphasized in My Comment at the bottom of the page in the December 14, 2022 post — We have reviewed many cases that illustrate the challenge posed by distinguishing between marked LVH vs LVH + superimposed acute OMI.
  • PEARL #1: In general, it is rare to see both marked LVH and acute OMI in the same tracing. It is for this reason — that we can get a "head start" in our interpretation of a patient with symptoms in which there is obvious LVH. This is because statistically (supported by our experience) — in the vast majority of cases, such tracings may mimic acute OMI, but acute coronary occlusion will rarely be seen.
  • PEARL #2: The above said — Remember the rule of "N = 1". By this I mean that even though it is rare to see an acute anterior OMI in a patient with marked LVH — this can occur — so that we want to be prudent and avoid overlooking the rare OMI in a patient with marked LVH (See the above mentioned December 14, 2022 post for a case in which marked LVH and acute OMI coexist).
  • BOTTOM Line: Awareness of the criteria for ECG diagnosis of LVH goes a long way toward facilitating interpretation. Toward this end — we've conveniently added a LINK for "LVH Criteria" in the Menu at the top of every page in Dr. Smith's ECG Blog. This link takes you to My Comment in the June 20, 2020 post — in which I review a user-friendly approach to ECG recognition of LVH and "Strain".

Figure-1: I've labeled today's ECG.

Regarding Today's CASE:
For clarity in Figure-1 — I've labeled today's tracing. 
  • The diagnosis of marked LVH should be obvious in Figure-1. That said — overlap of R waves with S waves in multiple leads (especially with the long lead rhythm strips at the bottom of the tracing) — complicates accurate determination of QRS amplitudes (See my color-coding in Figure-1 for my best effort at calculating R wave and S wave amplitudes in the various leads).
  • PEARL #3: The easiest way to avoid confusing lead overlap — is simply to repeat the ECG at half standardization. This was not done in today's tracing.
  • The most difficult beats to assess QRS amplitude on are beats #7,8,9 — because there is overlap with each of the 3 simultaneously-recorded long lead rhythm strips (of leads V1,II,V5). For example — true amplitude of the S wave in lead V3 is almost entirely concealed by overlap of both the lead V1 and lead II rhythm strips below it. In such cases of multiple lead overlap — I look elsewhere for leads with less overlap (ie, in leads II and V1, which are outlined in YELLOW and PINK) to determine the true amplitude of the S and R waves in these leads. This allowed me to determine that the S wave in lead V3 (in light BLUE) measures 36 mm deep!
  • PEARL #4: The KEY for determining that rather than "fulfilling STEMI millimeter-based criteria" for the amount of ST elevation in lead V3 — given the 36 mm deep S wave in this lead — this is in no way an "abnormal" amount of ST elevation (ie, the principle of "proportionality" reigns supreme for qualitative assessment of ST-T wave changes in a patient with marked LVH).
  • As to the straightened shape of the ST segment takeoff in lead V3 — this shape is completely consistent with the appearance of LV "strain" in an anterior lead in a patient with extremely deep anterior S waves (See My Comment in the February 6, 2020 post).

What About ST-T Wave Changes in Other Leads in Figure-1?
At 1st glance — the ST segment coving with seemingly "deep", symmetric T wave inversion in lead V5 might be of concern. That said — there are several reasons why I felt this ST-T wave appearance in lead V5 was not of concern:
  • Again, by the principle of "proportionality" — the 38mm tall R wave in lead V5 suggests the relative size of the inverted T wave in this lead is not as deep as one might initially think.
  • The slow downsloping, more rapid upsloping ST depression seen in lead V6 is absolutely typical for LV "strain" in this left-sided lead in which R wave amplitude is significantly increased (measuring 22 mm).
  • Patients with marked LVH (especially those with longstanding hypertension) often manifest not only ST-T wave changes that are typical for LV "strain" — but also symmetric T wave inversion as seen here in lead V5.
  • Finally — I interpreted the ST-T wave appearance in lead V5 as a "transition" lead that lies in between the ST coving and elevation seen in lead V4 — and the "strain"-like ST depression seen in lead V6. This ST-T wave pattern in lead V5 is not seen in other leads, as would be expected if this was truly a change of acute ischemia.

What about the R = S Phenomenon in the Inferior Leads?
I found the surprisingly tall R = S Waves in each of the inferior leads an interesting and unusual feature (R waves and S waves each ≥15 mm in leads II,III and aVF). I cannot remember the last time I saw this pattern in each of the 3 inferior leads.
  • This R=S pattern of tall RS complexes brings to mind the Katz-Wachtel phenomenon described in pediatric patients — in which the finding of biphasic RS complexes of ≥50 mm in mid-chest leads V2, V3 or V4 suggests biventricular hypertrophy, especially in children with VSD (Ventricular Septal Defect).
  • Clearly, the R=S waves in today's tracing are not as deep as occurs with the Katz-Wachtel phenomenon. That said, given the association of these inferior lead R=S waves with marked increase in chest lead amplitude — I would love to see an Echo on this patient, so as to correlate Echo findings with today's interesting ECG.

Conclusion:
The ECG in today's case is notable for marked LVH. As per Dr. Frick — this ECG is not suggestive of acute OMI. I attributed the diffuse ST-T wave changes to LV "strain" and not ischemia.


 





Monday, February 10, 2025

Potassium 6.2 with narrow QRS: any indication for calcium?

Written by Jesse McLaren

 

An 80 year old patient with diabetes/hypertension/cirrhosis had a recent increase in candesartan for their hypertension, and was also on spirolactone and nadolol. They presented to a hospital clinic for routine paracentesis, after which they developed nausea and syncope attributed to a vasovagal episode from the procedure. Labs showed a non-hemolyzed potassium of 6.2, normal glucose, and mild acute on chronic renal failure (Creatinine from 140 to 170 umol/L), and the following ECG, and they were sent to the ED. What do you think and how would you treat?






There’s sinus bradycardia, borderline PR interval, narrow QRS; normal axis/R wave progression; low precordial voltages, and subtle peaked T waves (most obvious in V2, but all T waves are symmetric with a narrow base). There’s no prior ECG to compare - but the bradycardia, prolonged PR and peaked T waves could all be from hyperkalemia. But does this patient with narrow complex ECG require calcium if the potassium is only 6.2?

 

The patient was seen three hours later in the ED, with triage vitals showing BP 50 and BP 106/60. There was no abdominal tenderness after paracentesis but the patient had ongoing nausea, and the following repeat ECG:




Slightly worse bradycardia but no other changes. Because of the narrow complex QRS and potassium of only 6.2 from the clinic, the patient was treated with fluids, insulin and dextrose but not calcium. ED labs showed a repeat K of 6.6 just as the patient was receiving their treatment, so no additional steps were taken.

Two hours later the patient became somnolent and the monitor showed the following rapid changes:


ECG after ROSC




Repeat K was 6.4 and the patient was given more insulin/dextrose/calcium and admitted to ICU. Follow up ECG showed resolution of sinus brady with ongoing PR prolongation:




Hyperkalemic ECGs and BRASH syndrome

This was my rude awakening years ago to the importance of ECG interpretation in hyperkalemia, and the dangers of the BRASH syndrome.

In med school and residency I’d been taught (and there are still multiple online examples of similar infographics) that the ECG in hyperkalemia goes through a gradual, progressive and predictable series of changes that correlate with serum potassium level – from peaked T waves at mild elevation, to loss of P wave and widening of the QRS at moderate elevation, then sine wave at severe elevation, and only then cardiac arrest. But this patient developed a deteriorating but persistent narrow complex brady-asystole preceded by only subtle ECG changes and with initial potassium of only 6.2. A good reminder of recommendations for calcium for either K>6 with any ECG changes (when the patient was first seen) or K>6.5 regardless of the ECG (when the repeat level came back).[1]

In a review of hyperkalemia in the ED, all adverse events occurred prior to calcium and usually with multiple signs of hyperkalemia (like the first ECG) – with the biggest predictors not only wide QRS, but also bradycardia and/or junctional rhythm.[2] Curiously, ACLS does not include consideration of calcium in its bradycardia algorithm, which could have prevented the arrest and which along with the epi produced ROSC.

Another learning point for me was the clinical deterioration out of proportion to the initial ECG and potassium level, which characterizes the vicious cycle of BRASH syndrome [3]. This patient had:

-    Bradycardia from the nadolol (and maybe worsened by vagal tone from the nausea 

         post-paracentesis), worsened by hyperkalemia, and contributing to shock  

-    Renal failure from the increase candesartan, worsening the hyperkalemia

-    AV nodal blockade from the nadolol, worsened by the hyperkalemia

-    Shock, from the bradycardia and hyperkalemia, worsening the renal failure

-    Hyperkalemia, from spirolactone/candesartan and new AKI, worsening all the above

In hindsight – and for future reference - a patient on AV nodal blocker and potassium sparing medication, presenting with bradycardia and a soft BP, and subtle hyperkalemic ECG changes is a classic candidate for BRASH syndrome – requiring immediate treatment of all the elements including calcium - even if only subtle ECG changes and moderate potassium level. And even without the subtle peaked T waves, bradycardia secondary to hyperkalemia is a high risk feature.

 

Take away

1.  Hyperkalemia can produce multiple abnormalities in rate/rhythm (including brady, junctional or wide complex rhythms), conduction (prolonged PR and QRS), axis, and repolarization abnormalities (including peaked T waves, or Brugada phenocopy) - and multiple abnormalities indicate high risk.

2. Hyperkalemia requires calcium if >6.5 regardless of the ECG, or >6 with any ECG  changes – with special attention to bradycardia, junctional rhythm, or wide QRS.

3. Consider BRASH syndrome which can produce clinical instability out of proportion to the ECG or potassium levels.

4. See below

See other cases of BRASH

 

Smith comments:


See Case 3 of this post, which demonstrates:

1) how easy it is to confuse the T-waves of Early repol from hyperkalemia and

2) how even with only peaked T-waves, HyperK can lead to ventricular fibrillation.

HyperKalemia with Cardiac Arrest. Peaked T waves: Hyperacute (STEMI) vs. Early Repolarizaton vs. Hyperkalemia


Recognize subtle findings of hyperK and, if present, treat with Calcium immediately!


References

1. Lindner et al. Acute hyperkalemia in the emergency department: a summary from a Kidney Disease: Improving Global Outcomes conference. Eur J Emerg Med 2020.

2. Durfey et al. Severe hyperkalemia: can the electrocardiogram risk stratify for short-term adverse events. West J Emerg Med 2017.

3. Farkas et al. BRASH syndrome: Bradycardia, Renal Failure, AV blockade, Shock, and Hyperkalemia. J Emerg Med 2020.






===================================
MY Comment, by KEN GRAUER, MD (2/10/2025):  
===================================
Today's case by Dr. McLaren serves as an important reminder of critical pitfalls in the treatment of hyperkalemia. 
  • In the interest of stimulating discussion — I focus my comments on some additional clinical implications of the initial ECG to those reviewed in the above discussion by Dr. McLaren.  

The diagnosis of hyperkalemia was never in question in today's case because: 
  • i) The initial ECG (reproduced in Figure-1) — strongly suggests significant hyperkalemia.
  • ii) The initial serum K+ = 6.2 mEq/L in a non-hemolyzed specimen. 
  • iii) The patient has multiple "predisposing conditions" for hyperkalemia. These include 3 medications known to potentially exacerbate hyperkalemia (ie, Aldactone — an ARB — and a non-selective ß-blocker) — with recent increase in the dose of the ARB Candasartan.
  • iv) This 80-year old patient with known diabetes, hypertension and renal insufficiency — has worsening renal function on this admission.

Today's Initial ECG in Figure-1:
The reason I interpreted the initial ECG as suggestive of significant hyperkalemia is because:
  • No less than 8/12 leads show characteristic T wave peaking (ie, with symmetric T wave ascent and descent, and a relatively narrow T wave base — in a "picture" resembling the tall, slender Eiffel Tower). That is, despite relatively reduced amplitude of these T waves (ie, the only really tall T wave is in lead V2) — overall QRS voltage is so low, that 6 of these 8 leads with peaked T waves manifest T wave amplitude equal to or greater than R wave amplitude in the corresponding lead.
  • In addition — there is bradycardia with a borderline PR interval prolongation.

Two additional ECG findings in Figure-1 "caught my eye":
  • The ST segment is surprisingly flat in all 12 leads! (Blue arrows highlight this ST segment flattening in leads V4,5,6 — but this finding is seen virtually everywhere! ).
  • As I emphasized in the March 19, 2019 post — the characteristic ECG picture of hypocalcemia is that of a flat and prolonged ST segment, at the end of which occurs a surprisingly normal-looking T wave. But this "normal" T wave appearance of hypocalcemia may be altered if the patient also has hyperkalemia (and both hyperkalemia and hypocalcemia are often seen together in renal failure). 
  • So while the QTc interval is not actually prolonged in Figure-1 — it "looks" prolonged because of how flat the ST segments are (such that this ECG picture of long, flat ST segments followed by T wave peaking should suggest possible associated hypocalcemia). The reason this is clinically important — is that if hypocalcemia is present, this may further exacerbate the adverse cardiac effects of hyperkalemia (Barboza de Oliveira et al — Rev Bras Cir Cardiovasc 29(3):432-436, 2014).
  • This is relevant to today's case — because the ECG in Figure-1 manifests low voltage (No limb lead QRS greater than 5 mm — and except for lead V2, surprisingly low QRS amplitudes in the other 5 chest leads). As I noted in the November 12, 2020 post — among the causes of low ECG voltage is depressed LV function, which could further potentiate the above list of factors predisposing to cardiac decompensation.

Figure-1: The initial ECG in today's case.


WHY Isn't the QRS Wide?
As per Dr. McClaren — the "textbook" sequence of ECG findings seen with progressive degrees of hyperkalemia is not seen in all patients. As I emphasized in My Comment in the February 27, 2023 post in Dr. Smith's ECG Blog — some patients may develop everything except QRS widening. Others may not show T wave peaking — or may only show this finding as a later change. And despite marked hyperkalemia — some patients may not show any ECG changes at all
  • So while I still feel it helpful to be familiar with the sequence of "textbook ECG changes" of hyperkalemia (that I review in that Feb. 27, 2023 post) — it's essential to appreciate that a significant percentage of hyperkalemic patients do not read the textbook!

But the Serum K+ is "only" 6.2 mEq/L ...
As emphasized by Dr. McLaren — this level of hyperkalemia is sufficiently high to predispose to clinical decompensation unless treated with IV Calcium because:
  • Bradycardia is a major predictor of adverse events in patients with hyperkalemia.
  • This 6.2 mEq/L level is associated with ECG abnormalities.
  • The vicious cycle of "BRASH" Syndrome is operative.

To this — I'd add the following: 
  • Some patients with significant hyperkalemia potentially causing severe rhythm disturbances do not develop any ECG abnormalities at all.
  • Rather than the numerical value of serum K+ — it is the rate of change in serum K+ levels that is more important as a predisposing factor for hemodynamic deterioration (Simon et al — StatPearls, 2023). Today's case features many factors predisposing to potentially rapid K+ ion shifts between intra- and extracellular compartments.
  • Did the patient also have hypocalcemia?
  • Was LV function already depressed before onset of the vicious cycle of BRASH Syndrome changes?


 



Saturday, February 8, 2025

‘NSTEMI’ or reperfused OMI? And which lesion is the culprit?

Written by Jesse McLaren

 

An 80 year old with a history of CHF, ESRD on dialysis, and multiple prior cardiac stents presented to the emergency department with 3 days of intermittent chest pain and shortness of breath that resolved after nitro, which felt like prior episodes of angina. The patient was pain free on arrival, and below are the prior and new ECG. What do you think?


Prior on top, New on bottom




 

 

 

There’s normal sinus rhythm, normal conduction, left axis, poor R wave progression and low precordial voltages. Compared with prior there are subtle T wave inversion inferior and lateral. In a patient with resolved ischemic symptoms this suggests infero-lateral reperfusion, usually from the RCA vs left circumflex.


Smith: I looked at the bottom ECG without even looking at the previous, and could see that there is classic morphology of reperfusion, especially in lead III, with recriprocal STD and upright (reciprocal reperfusion) T-wave in aVL.  Then when you compare with the old ECG, the change makes it diagnostic of inferior and lateral reperfusion.

 

 

‘NSTEMI’ or reperfused OMI?

 

The emergency physician ECG interpretation was simply “NSR”. When the hs-troponin I returned at 475 ng/L (compared to baseline of 60), the patient was referred to cardiology as “NSTEMI.” The cardiology interpretation was “left axis, anteroseptal Q, poor R wave progression”, and the patient was admitted as “NSTEMI”. This implies a non-occlusive MI that can safely wait for delayed angiogram.

 

But even without comparison to the prior ECG, the Queen of Hearts identified the ECG as showing reperfused OMI, at risk for reocclusion:


Smith: You can see that the Queen of Hearts sees leads III and aVL just like I did.


What’s the culprit?

 

The next day the patient went to the cath lab, where the interventional cardiologist noted: “ECG did not reveal any acute ischemic changes. There appeared to be Q waves both in the inferior and anterior leads. Reviewing his old ECGs as well there were no significant changes compared to previous.” Angiogram showed a chronic total occlusion of the circumflex, multiple patent stents, and two stenoses: 95% distal RCA and 90% mid LAD.




 

So which was the culprit? As the cath lab report noted, “The culprit vessel unfortunately was not clear due to the fact that he has diffuse coronary artery disease. It is possible either the LAD or RCA is contributing to his presentation. I suspect the RCA lesion is also chronic. His ECG was unfortunately not helpful given it had evidence of Q waves anteriorly as well as Q waves inferiorly on some of the ECGs in the past. We agreed that it was reasonable to revascularize the LAD.”

 

In other words, because the subtle inferior reperfusion was not identified, the culprit RCA was not stented. Over the next couple of days the patient continued to have intermittent chest pain.

 

A few hours after angiogram the patient developed chest pain:





Now the previously inverted infero-posterior T waves are upright (pseudonormalization), and there is reciprocal ST depression in aVL which is highly specific for inferior OMI. The patient has spontaneously re-occluded.

 

Queen of Hearts of Heart identifies this as acute coronary occlusion:





The chest pain resolved after nitro and the ECG was not repeated.

 

The next day the patient had another episode of pain that resolved before assessment:



Reperfused again



The following day the patient had another episode of chest pain:





Spontaneously re-occluded again. This was interpreted as "inferior STEMI" and the cath lab was activated. At the time of the angiogram the RCA was again open at 95%, and stented. Troponin rose from 380 ng/L to 930 ng/L before cath, but was not repeated after. The patient had no further episodes of chest pain.

 

Next day ECG showed reperfusion.





Discharge diagnosis was ‘Non-STEMI’.

 

Here are the ECGs again, focusing on the inferior leads and reciprocal change in aVL:





Take home

1.        The catch-all phrase ‘NSTEMI’ does not differentiate between different pathologies with different management based on the state of the coronary artery: non-occlusive MI (non urgent cath), subtle occlusion MI (emergent cath), and reperfused occlusion at risk of re-occlusion (urgent cath)

2.        The STEMI/NSTEMI dichotomy can make it difficult to identify the culprit lesion, which can be spontaneously reperfused at the time of the angiogram

3.        T waves are very specific markers for the dynamic process of spontaneous reperfusion/re-occlusion

4.        The Queen of Hearts can differentiate subtle reperfused OMI from NOMIs, and help guide cath lab decisions

5.        Further significant myocardial damage could have been avoided by stenting the RCA at the first cath, but this is only possible with accurate ECG interpretation, or with use of the Queen of Hearts.






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

MY Comment, by KEN GRAUER, MD (2/8/2025):
===================================
Important case presented today by Dr. McLaren — because it highlights the misinterpretations and misconceptions that continue to be all-too-common in everyday practice.
  • To facilitate comparison in Figure-1 — I've reproduced the prior (baseline) ECG on today's patient — together with the initial ECG recorded in the ED.

My Concerns Regarding this CASE:
  • The History was Ignored: Today's patient is an 80-year old with known coronary disease — who presents with 3 days of intermittent CP (Chest Pain) — but who was not having any CP on arrival. Embedded in this history are 3 reasons for the ED physician to suspect that any ECG abnormalities that might be seen could be subtle: i) The patient is older with a history of multiple prior stents — therefore highly likely to have significant underlying heart disease (probably multi-vessel) — with potential for significant collateral flow that may attenuate the prominence of new changes; ii) The patient's CP has been intermittent — therefore potential for new ECG changes to be in a state of transition (ie, pseudo-normalization) between the stage of ST elevation and the stage of reperfusion ST depression/T wave inversion; andiii) The patient's CP has resolved at the time the initial ECG was recorded (which often results in significant reduction, if not elimination of ST-T wave changes).
  • Saying the Elevated Troponin was the Result of a NSTEMI: The combination of the history of CP + ST-T wave abnormalities consistent with reperfusion changes (especially in comparison to a prior tracing without such changes) + significant Troponin elevation — is diagnostic of an OMI. As per Dr. McLaren — misdiagnosing today's case as a "NSTEMI" only serves to delay the need for catheterization (at the potential price of losing more myocardium).
  • Key ECG Findings in Figure-1 were Missed: — i) Which leads in ECG #1 were misplaced? — andii) What important new findings are revealed by lead-to-lead comparison between ECG #1 and ECG #2?

Figure-1: Comparison between the initial ED ECG — with the prior ECG on this patient.


KEY ECG Findings in Figure-1 that were Missed:
It is because the history in today's case so strongly suggests that this 80-year old patient with 3 days of intermittent CP that is no longer present might only manifest subtle ECG abnormalities — that lead-to-lead comparison between ECG #1 and ECG #2 is so important. Without using this simple technique of lead-to-lead comparison — it becomes all-too-easy to miss real but subtle differences between the 2 tracings.
  • Comparison between ECG #1 and ECG #2 needs to take into account that the lead V1 and V2 electrodes have been placed too high on the chest in ECG #1. We can instantly recognize this because: i) There is such a deep negative component to the P wave in both of these leads; — ii) There are terminal r' deflections in both V1 and V2; — andiii) The PQRST complexes in leads V1,V2 look very much like the PQRST complex in lead aVR (See My Comment in the November 4, 2018 postamong many others).
  • Turning my attention to ECG #2 — my "eye" was immediately drawn to the 2 leads within the RED rectangles ( = leads III and aVF) — because these leads show: i) Abnormal ST segment coving, with a hint of slight ST elevation; — ii) Terminal T wave inversion, which in association with ST coving that shows no more than minimal ST elevation — is suggestive of some spontaneous reperfusion; — iii) Subtle "scooping" of the ST segment in high-lateral leads I and aVL — which is consistent with subtle reciprocal ST-T wave changes; — andiv) The absence of these ST-T wave changes in these 4 leads on the prior tracing!
  • Looking at the chest leads in ECG #2 — similar subtle-but-real ST segment coving occurs, as was seen in leads III,aVF — here, with a hint of ST elevation in lead V5 — with terminal T wave inversion in leads V5,V6. This suggests recent lateral OMI, now with suggestion of some spontaneous reperfusion.
  • Knowing that infero-lateral OMIs are so often accompanied by posterior wall involvement — I interpreted the subtle lack of gently upsloping ST elevation in lead V2 as consistent with the overall picture of recent infero-postero-lateral OMI, most probably with some pseudonormalization and the beginning of reperfusion T waves.

BOTTOM Line: The history in today's case alerts the informed provider to the type of subtle ECG findings that need to be looked for.
  • The finding of a significantly elevated initial Troponin ( = 475 ng/L) confirms the diagnosis of recent (and/or ongoing) coronary occlusion ( = an OMI) — until proven otherwise. To call this a "NSTEMI" — is to delay needed catheterization and the chance to salvage viable myocardium.
  • ECG findings on the initial ECG are subtle. But IF the informed provider assesses this initial tracing by lead-to-lead comparison with the prior ECG — definite ST-T wave changes will be seen in at least 6/10 leads (with comparison of leads V1,V2 between these 2 tracings invalidated by too-high-placement of these leads in ECG #1)




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