Friday, February 14, 2025

A man in his 30s with epigastric pain and chest pressure

Written by Pendell Meyers


A man in his 30s presented with acute upper midline abdominal pain and nausea. He described it as radiating into his chest, like "pressure", and "burning". 

Vitals were within normal limits except bradycardia. Here is his triage ECG:

What do you think?





Sinus bradycardia, normal QRS. There is STE in several leads including I, aVL, and V2, with STD in II and aVF. The question is whether this is due to OMI, or not. If it were due to OMI, it would fulfill the "South African Flag" pattern.

Unfortunately, presence of reciprocal depression does not ensure that STE is due to OMI. 


I sent this ECG with zero other information to Dr. Smith and Dr. Frick, both said it was an OMI mimic (meaning they do not think that the STE in I, aVL, V2, etc, is due to acute coronary occlusion, but rather a normal variant). I agreed, there is something about the morphology (including the J waves, but not limited to that) that doesn't match prior OMIs in my experience, and does match prior normal variants. 

PM Cardio QOH says No signs of OMI.

The ECG meets STEMI criteria objectively.




The ED physician did not think the ECG represented OMI.

Two serial high sensitivity troponin T levels were undetectably low (less than 6ng/L). AMI was ruled out.

One other ECG was obtained during the ED stay:






The patient was discharged home. No further follow up is available.



Compare this case with similar OMIs and OMI mimics:

Quiz post - which of these, if any, are OMI? What is the South African Flag Sign? Will you activate the cath lab? Can you tell the difference on ECG?


Quiz post: do either or both of these patients have high lateral OMI / South African flag sign?








===================================
MY Comment, by KEN GRAUER, MD (2/14/2025):
===================================
I find cases like today's challenging. My answers usually take 1 of 3 forms: i) That the initial ECG is diagnostic or strongly suspicious of acute OMI until proven otherwise; — ii) That the initial ECG is simply not suggestive of anything acute; — or — iii) That I do not think the initial ECG represents an acute OMI — but I would not send the patient home on the basis of this single ECG.
  • For me, today's initial tracing best fits in Category iii) — in that I did not think this tracing represents an acute OMI — but that I would want more information before sending the patient home.

For clarity in Figure-1 — I've labeled today's initial ECG to highlight the findings that "caught my eye".

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

Today's Initial ECG:
For an otherwise presumably healthy 30-year old man — there are some unusual findings in ECG #1. These include the following:
  • A fairly marked sinus arrhythmia with bradycardia, and almost the pattern of "group" beating in the long lead rhythm strip. P wave amplitude is reduced in virtually all leads — with comparable small size of the upright P waves in lead I as in lead II, making me question whether this truly is a sinus rhythm? — vs a low atrial rhythm? — vs the possibility of LA-LL Reversal? (See My Comment in the June 25, 2024 post for changes with LA-LL reversal). The above said — this is not necessarily an abnormal rhythm in a young adult.
  • A 4-component rSR's' complex in lead V1. This is not a simple incomplete RBBB pattern, which should only consist of 3 components without a terminal s' deflection.
  • A slender, but unusually deep Q wave in lead III (that is over 5 mm deep). Narrow Q waves are also seen in leads aVF and V6.
  • Prominent J-point notching in leads I and aVL. These look a bit unusual, because we are not accustomed to seeing such deep S waves in these high-lateral leads. That said — this notching is usually a benign feature of repolarization variants, especially when associated with no more than modest ST elevation associated with an upward concavity (ie, "smiley" configuration), as seen here.
  • From the perspective of a patient presenting to the ED with abdominal pain radiating to the chest — I found the flat (shelf-like) ST depression in lead aVF to be the most concerning feature in this tracing.
  • J-point depression with a downsloping ST segment and biphasic T wave in lead III would have added to my concern if this ST-T wave picture in lead III was not the exact mirror-image opposite of what I perceived to be a benign picture of prominent J-point with smooth, upsloping ST elevation in lead aVL.
  • Finally, though not more than minimally depressed — the flattened ST segment in lead V6 could be complementary to the ST depression seen in lead III.

Putting It All Together: 
I thought the initial ECG in today's case was not "normal" for a man in his 30s.
  • I did not think this initial tracing represented an acute OMI — because of the benign-looking appearance of J-point notching with upward sloping ST elevation in leads I,aVL.
  • I wondered if some of the unusual QRS features in the limb leads could be the result of LA-LL reversal — so I would verify lead placement.
  • That said — a form of limb lead reversal would not alter the 4-component rSR's' complex in lead V1, so the leads may be correctly placed.
  • I'd want to know about the patient's body habitus (as possible explanation for some of the less usual ECG features).
  • And then, I am left with that shelf-like ST segment depression in lead aVF — that is not usually part of the picture of a repolarization variant. And this patient did present to an ED with new symptoms of a "pressure" that radiates to the chest. Primarily for this reason — I was less than 100% certain about the diagnosis.
  • BOTTOM LINE: I did not think ECG #1 represented an acute OMI. That said — I was less than 100% certain of that on the basis of the single initial ECG. As a result — I would: i) Repeat the ECG after verifying lead placement; — ii) Rule out acute OMI with 2 serial Troponins, as was done; — and, iii) Get an Echo to rule out any unexpected underlying structural disease (I find it insightful to always try to better understand why a non-OMI ECG may have unexpected features)


 





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.




===================================
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 presented to a hospital clinic for routine paracentesis, after which they developed nausea and syncope attributed to a vasovagal episode from the procedure. 


They had a recent increase in candesartan for their hypertension, and was also on spirolactone and nadolol.


An ECG was recorded:


What do you think?






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. 


Smith: Hyperkalemia T-waves do not need to be tall; they simply have a narrow base which is a major contributor to their peaked appearance. These T-waves have a narrow base and are peaked but not tall.


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?


 



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