The Queen always asks (if she sees OMI) "Is there a clinical suspicion of acute coronary syndrome"

This was sent by Asad Tasleem, an Emergency Medicine resident in Pakistan:

"I am an ED Resident in a tertiary care Hospital Pakistan.  I received a 70 year old male with DM, HTN who presented with history of fall of unknown mechanism possible syncopal episode.  On arrival he was vitally stable and all of the attention was to the obvious deformity of hhis left leg which turned out to be a femoral neck fracture. 

I ordered an EKG: 

What do you think?

There is ST Elevation in V2-V4 which does NOT meet STEMI criteria.  But that STE is in the context of a very low R-wave and QRS voltage (amplitude).  Thus, it is ST Elevation out of proportion to the QRS.  This is diagnostic of acute LAD Occlusion.  Asad Tasleem recognized it immediately.

I sent it to the PMCardio Queen of Hearts AI ECG model.  The Queen always asks about the pretest probability, because that is crucial to any test, and it is quite possible that an ECG which appears to represent OMI does NOT represent OMI if there is a very low pretest probability.

I answered "No" to the question.

You can see that, in spite of the "No" answer, she is still worried about OMI 

Asad continues:

"I thought it was very suspicious for Terminal QRS distortion in anterior leads.  I rushed cardiology and as always they weren't convinced as the patient had no chest pain.  Trop came positive and continue to rise on serial tests."

_____

Smith: strictly speaking, "terminal QRS distortion" is only proven to be highly specific for LAD OMI if it is in leads V2 or V3.  However, it likely a significant finding in V4. 

_______

Smith response:

"It sure looks like OMI to me.  If there are no symptoms of myocardial ischemia, one must be skeptical, of course. But one must also explain the EKG findings. It looks like OMI and the queen agrees.  How high did the troponins go?"

Smith comment: One must assume OMI until proven otherwise, and DO NOT wait for troponins.

Asad Response: hs Troponin I went from 2000ng/L to 8000ng/L to 10000ng/L.

______

Later, he found a subsequent ECG.  It is not certain when it was recorded.  

Now there can be no question of LAD Occlusion, even if the patient has no symptoms, or only toe pain.

Nevertheless, it did not motivate the cardiologists to take him to the cath lab.

Several days later, he did go to the cath lab and a 100% LAD Occlusion was found

Learning Points:

1. Patients can have large acute Occlusion MI without any symptoms.

2. If the ECG shows unequivocal OMI, then you need to do an angiogram even if there are no relevant symptoms.

3. Silent MI is very common, though it is almost always found days, weeks, months, or years after the event via tests done for other reasons, in which they find Q-waves on the ECG, or wall motion abnormality on echo.  It is less common to find it via ACUTE ECG findings in an acute situation, but as you see it can happen.

4. Acute MI without chest pain, but presenting with other symptoms, is very common, approximately 33% for both STEMI and Non-STEMI (a term that I can't stand!).

Canto JG, Shlipak MG, Roger WJ. Prevalence, clinical characteristics, and mortality among patients with myocardial infarction presenting without chest pain. JAMA 2000;283(24):3223–9.    

See this paper on Silent Myocardial Infarction:

Qureshi WT, Zhang Z-M, Chang PP, et al. Silent myocardial infarction and long-term risk of heart failure: The ARIC study. J Am Coll Cardiol [Internet] 2018;71(1):1–8. Available from: http://dx.doi.org/10.1016/j.jacc.2017.10.071   

Full text link to pdf.

Abstract

Background:

Although silent myocardial infarction (SMI) accounts for about one-half of the total number of myocardial infarctions (MIs), the risk of heart failure (HF) among patients with SMI is not well established.

Objectives:

The purpose of this study was to examine the association of SMI and clinically manifested myocardial infarction (CMI) with HF, as compared with patients with no MI.

Methods:

This analysis included 9,243 participants from the ARIC (Atherosclerosis Risk In Communities) study who were free of cardiovascular disease at baseline (ARIC visit 1: 1987 to 1989). SMI was defined as electrocardiographic evidence of MI without CMI after the baseline until ARIC visit 4 (1996 to 1998). HF events were ascertained starting from ARIC visit 4 until 2010 in individuals free of HF before that visit.

Results:

Between ARIC visits 1 and 4, 305 SMIs and 331 CMIs occurred. After ARIC visit 4 and during a median follow-up of 13.0 years, 976 HF events occurred. The incidence rate of HF was higher in both CMI and SMI participants than in those without MI (incidence rates per 1,000 person-years were 30.4, 16.2, and 7.8, respectively; p < 0.001). In a model adjusted for demographics and HF risk factors, both SMI (hazard ratio [HR]: 1.35; 95% confidence interval [CI]: 1.02 to 1.78) and CMI (HR: 2.85; 95% CI: 2.31 to 3.51) were associated with increased risk of HF compared with no MI. These associations were consistent in subgroups of participants stratified by several HF risk predictors. However, the risk of HF associated with SMI was stronger in those younger than the median age (53 years) (HR: 1.66; 95% CI: 1.00 to 2.75 vs. HR: 1.19; 95% CI: 0.85 to 1.66, respectively; overall interaction p by MI type <0.001).

Conclusions:

SMI is associated with an increased risk of HF. Future research is needed to examine the cost effectiveness of screening for SMI as part of HF risk assessment, and to identify preventive therapies to improve the risk of HF among patients with SMI.

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MY Comment, by KEN GRAUER, MD (5/8/2025):

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Today's patient is a 70-year old man who presented to the ED (Emergency Department) with a history of a fall of unknown mechanism, with possible syncope — that resulted in a hip fracture. Of note — this patient never complained of CP (Chest Pain).

• Credit to Dr. Tasleem: i) For reviewing this patient's ECG as soon as he was assigned to this patient's care (which apparently was the morning after the patient was admitted to the hospital for his hip fracture) and, ii) For recognizing T-QRS-D (Terminal-QRS-Distortion) and other ECG findings indicative of acute infarction that Dr. Tasleem immediately brought to the attention of the Cardiology team.

The above said — A series of oversights in today's case merit discussion. These include the apparent failure of anyone (other than Dr. Tasleem):

• i) To consider the importance of trying to determine WHY this 70-year old man fell (especially given the inability by history to exclude syncope as the cause of his fall).
• ii) To appreciate that acute MI may occur with surprising frequency in the absence of chest pain.
• iii) To look at this patient's initial ECG (that I've reproduced in Figure-1) — or, if someone did look at ECG #1 — then the abnormal ECG findings went unrecognized (and this abnormal initial ECG was not repeated until too much time later).
• iv) To process potential clinical implications of this patient's progressively increasing Troponin values (from 2,000 — up to 10,000 ng/L) — such that cardiac catheterization was not done until days after these elevated troponin levels were known.

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Lessons to be learned ...

• The entity of "Silent" MI is not new — having been documented over 40 years ago in the Framingham Studies (See My Comment in the December 6, 2022 post, among other posts).
• Depending on which study in the literature is cited (and depending on which study methods were used) — at least 1/4 to 1/3 of all MIs occur without CP.
• Editorial Comment #1: I suspect that literature figures on the frequency of "silent" MI have been underestimated because: i) Coding methods have often been used as the way to document infarction in the absence of CP; and, ii) The concept of STEMI-negative acute coronary occlusion (ie, acute "OMI" ) — was unknown at the time older studies estimating the frequency of MI-without-CP were done — and even today, the OMI Paradigm remains unappreciated by all-too-many clinicians.

Editorial Comment #2: Realizing imperfect methodology of the literature we have — the bottom line is that MI-without-CP is a surprisingly common phenomenon. I still favor the Framingham data (Kannel & Abbott: N Engl J Med 311(18):1144-1147, 1984 — and — Kannel: Cardiol Cin 4(4):583-591, 1986) — because of the clinically insightful breakdown by these authors of patients found to have MI-without-CP:

• About half of the patients in Framingham who were found to have MI-without-CP — had no symptoms at all, therefore truly "silent" MIs.
• The other half of patients who had MI-without-CP — had "something else" as a "CP-equivalent" symptom (ie, shortness of breath — abdominal pain — "flu-like" symptoms — excessive fatigue — syncope — mental status changes).
• 
  
• KEY Point: The 70-year old man in today's case falls into this latter group — in that he had an unexplained fall that was serious enough to result in a hip fracture — and without recollection of whether he tripped or suddenly fainted.
• BOTTOM Line: The history in this case should immediately prompt inclusion of a cardiac arrhythmia and/or acute infarction as a potential cause of a potential "silent" MI — for which the initial ECG is probably the most important 1st test to be done (and immediately reviewed by the treating physician as soon as the ECG is recorded).

Review of Today's Initial ECG:

For clarity in Figure-1 — I've put both of today's tracings together.

• In ECG #1 — My "eye" was immediately drawn to leads V4 and V5 (within the RED rectangle). Regardless of the absence of CP — acute LAD occlusion should be assumed until proven otherwise given: i) Significant coved ST elevation in these leads; ii) T-QRS-D (YELLOW arrows in these leads); and, iii) Small but clearly abnormal Q waves in both leads V4 and V5.
• Neighboring leads V3 and V6 support our strong suspicion for an acute event — given ST segment straightening and elevation in lead V3 — and the Q wave with hyperacute and elevated ST segment in lead V6.
• Note #1: Although data by Drs. Smith and Meyers in support of the diagnostic value of T-QRS-D is from identification of this phenomenon in lead V2 and/or V3 — cases like today suggest the phenomenon is also most probably valid when seen in lead V4 (and perhaps ? in lead V5 — at least for today's case).
• Note #2: BLUE arrows in ECG #1 highlight Q waves in each of the inferior leads.  That said — baseline artifact and what appears to be nonspecific ST-T wave flattening in virtually all limb leads impedes determination of whether inferior MI is old or possibly new.

Figure-1: Comparison between the 2 ECGs in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

The Repeat ECG:

As per Dr. Smith — comparison of ECG #2 with ECG #1 in Figure-1 leaves no doubt that acute LAD occlusion is actively ongoing (which was finally confirmed by cardiac cath done too many days after hospital admission).

• Note further loss of QRS amplitude in ECG #2 — with development of a QS complex in lead V3, deepening of lateral chest lead Q waves — and now even more marked ST elevation in lead V4 (There has been "loss of R wave" from lead V2-to-V3 — with development of the deep QS in lead V3).
• While still impossible to tell without a previous ECG for comparison — I found it of interest that ST elevation is now seen in lead II of ECG #2, and to a lesser extent in lead aVF — suggesting inferior wall involvement, as well as the extensive anterior STEMI.

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ADDENDUM:

It's important to be aware of the concept of Terminal QRS Distortion (T-QRS-D). While not needed for the diagnosis of acute LAD OMI in today's case — there are times when recognition of T-QRS-D may provide invaluable assistance for distinguishing between early repolarization vs acute OMI (ie, When true T-QRS-D is present in a patient with new symptoms — it is virtually diagnostic of acute OMI). To review:

• T-QRS-D — is defined as the absence of both a J-wave and an S-wave in either lead V2 or lead V3 (and according to Drs. Smith and Meyers — probably also in lead V4). Although simple to define — this finding may be subtle! I fully acknowledge that it has taken me a while to become comfortable and confident in its recognition.

A picture is worth 1,000 words. I’ve taken the lead V3 examples in Figure-2 from previous cases posted on Dr. Smith’s ECG Blog:

• TOP in Figure-2 — Despite marked ST elevation in this lead V3 — this is not T-QRS-D, because there is well-defined J-point notching (BLUE arrow). This patient had a repolarization variant as the reason for ST elevation.
• BOTTOM in Figure-2 — This is T-QRS-D, because in this V3 lead there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline).

Figure-2: Comparison between ST elevation in lead V3 due to a repolarization variant (TOP — from 4/27/2019) — vs acute OMI (BOTTOM — from 9/20/2015), which manifests T-QRS-D (This Figure-2 is from My Comment in the November 14, 2019 post).

 

Seizure and Tachycardia

This was written by one of our fantastic Emergency Medicine 3rd year residents, Emily Ferrari:

A young man presented with AMS and seizure like activity. EMS called by PD from a scene, where the patient had been seen ingesting powder and pills, then began acting more erratically. He was seizing on arrival to the ED, but this ceased after 5mg Versed given by medics. 

Once on the monitor, he had an odd appearing QRS complex, consistent with wide complex sinus tachycardia. We called for ECG, and while exposing the patient during our secondary survey - he notably had a large amount of white powder in a baggy but also free form around his genitalia...

His first ED ECG as below :

What do you think?

Sinus rhythm.  Now borderline tachycardic.  A very wide QRS (178ms), large R-wave in aVR, and Brugada morphology in V1-V2.  

This is typical Sodium channel blockade morphology.  One might appropriately be worried about hyperkalemai, but this ECG is so pathognomonic of Na channel blockade that one should immediately administer the antidote, which is Na-bicarbonate.

What specific drugs/medications do this?  

1. Tricyclic antidepressants.

2. Type 1 antidysrhythmics, especially flecainide.

3. Cocaine

With the reported ingestion of the white powder, and seizure, there was strong suspicion of cocaine toxicity in this patient (in other settings, we would need to be cognizant of possible TCA overdose). 

An IV was placed, and bloods were drawn, including a venous blood gas.

He was immediately given 2 "amps" of sodium bicarbonate (100 mL of 8.4% NaHCO3 = 100 mEq of Na and 100 mEq of HCO3), with the resulting ECG: 

The QRS is now 160 ms

The Brugada pattern persists

His initial venous blood gas returned with pH 6.96, pCO2 64, pO2 84, bicarb 14.

We continued with serial administration of 2 doses of bicarbonate, with the following ECGs showing narrowing of his QRS to 130 ms:

Another VBG returned with 7.21/47/67/18

And with more bicarbonate, the QRS normalized:

QRS is now 110 ms, upper limit of normal

The patient required intubation for airway protection and concern for concomitant respiratory acidosis and persistent stupor. A bicarbonate drip was ordered, but subsequently not used as his QRS remained normal. Later, his urine drug screen was positive for both cocaine and fentanyl, and he was discharged from the ICU three days later. 

Reminders about pathognomonic ECG patterns in Sodium Channel Blockade:

1. R-wave in aVR that is > 3mm or an R:S > 0.7 is highly suspicious for sodium channel blockade. 
2. In  TCA overdoses, QRS duration > 100ms is 100% sensitive for detecting patients that are high risk for seizure, though this is specifically noted in. 

Notably this patient also had a drug-induced Brugada pattern in V1 and V2. Dr. Smith has noted this phenomenon in a previous blog post. 

Follow up ECGs:

A few more Cases:

Cardiac arrest, severe acidosis, and a bizarre ECG

A Patient with Cocaine Chest Pain and Prehospital Computer interpretation of ***STEMI***

Brugada pattern induced by tricyclic antidepressant

Pre-syncope and a bizarre wide complex

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MY Comment, by KEN GRAUER, MD (5/6/2025):

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Today's case by Dr. Smith is another "must know" for emergency providers — in that the history of seizures and the initial ECG (that I've reproduced in Figure-1) means that we need to immediately consider any toxicity producing Sodium-Channel Blockade (ie, tricyclic antidepressant overdose; proarrhythmia from antiarrhythmics such as flecainide or procainamide — or other agent listed in the excellent reviews by Dr. Ed Burns from Life-In-The-Fast-Lane or by Josh Farkas in the Internet Book of Critical Care).

• As shown above by Dr. Smith — serial treatment with Sodium Bicarbonate typically produces rapid clinical improvement.

As a visual reminder — ECG #1 shows the characteristic signs of Sodium-Channel Blockade:

• Sinus Tachycardia.
• QRS prolongation to ≥0.10 second (It is especially the terminal portion of the QRS that is prolonged with sodium channel blockade). QRS morphology may look bizarre.
• QT prolongation (the result of slowed ventricular depolarization).
• Terminal RAD (Right Axis Deviation) — as is characteristically manifest by a terminal S wave in lead I (that may be wide) — and/or — a significant terminal R wave component to the QRS complex in lead aVR (that is uaully ≥3 mm in amplitude). These effects are thought to be due to slow conduction through the myocardium, leading to delayed depolarization of the RV (therefore the last vector of ventricular depolarization is directed to the right).
• Brugada Phenocopy.

NOTE: The ECG of a patient with sodium channel blockade may resemble that of hyperkalemia (bizarre, widened QRS, right axis, Brugada-1 ECG pattern). 

• Both of these entities may be present at the same time — such that both empiric IV Calcium and IV Bicarbonate may be tried until definitive diagnosis is made.

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