Saturday, January 22, 2022

A man in his 40s with chest pain and T wave inversion

Written by Pendell Meyers with edits by Smith


A man in his early 40s with history of HTN presented to the ED for feeling lightheadedness and mild "beating" chest pain off and on last night, but resolved at the time of ED presentation. He still felt some lightheadedness during evaluation. He stated that he used ecstasy yesterday prior to the onset of symptoms. Vitals were within normal limits on arrival.

Here is his ED ECG on arrival:

What do you think?














Sinus rhythm. The narrow QRS with relatively high voltage is overall most consistent with a young healthy heart, less likely pathologic LVH (including HOCM). There are no signs of OMI or hyperkalemia. There are terminal T wave inversions present in V3 and V4. 

Most learners will not be able to distinguish these TWIs from Wellens' waves. But they are distinctly different and it is difficult to describe why we can tell that they are different. The morphology of the QRS complex itself helps me recognize this overall pattern.

First: What is Wellens' Syndrome?  It is: 1) An episode of anginal chest pain that has resolved, or is resolving. 2) An ECG that has preserved R-waves in V2-V4.  3) The ECG shows terminal T-wave inversion in some or all of V2-V4 ("Pattern A") or deep symmetric T-wave inversion ("Pattern B").  But not all T-wave inversions are equal!

This case and ECG was sent out to our little group of EKG nerds and all immediately recognized it as a normal variant, NOT as Wellens' syndrome.

Young people, especially men, can have a wide range of normal variants including normal variant STE ("early repol", etc.) and normal variant TWI ("persistent juvenile T wave pattern", "benign T wave inversion pattern", etc.). Unfortunately for learners, all of these patterns can change over time. Difference from a baseline ECG does not rule out a normal variant pattern.

This pattern in the ECG above does not fit perfectly into a described variant (it approaches the category of benign T wave inversion pattern), but I have seen many cases like it.

Here are some examples of true Wellens (anterior reperfusion) T waves (the first case will make some readers quite irritated because it looks so similar to the case above, but I promise with time and experience they look different):







A 40-something healthy male with transient chest squeezing




Classic Evolution of Wellens' T-waves over 26 hours





Back to the case:


The patient had a prior ECG on file from 6 months ago:

No TWI here. Tiny amount of normal variant STE in lateral leads. 


It is certainly appropriate to measure troponins, and so 3 serial high sensitivity troponin I measurements were all ⋖ 6 ng/L (below the limit of detection, normal 99% URL for men for this assay is 20 ng/L).


Repeat ECG 4 hours after arrival:

The T wave may be a tiny bit deeper in V3, but overall there is not much change.

Side by side is below.


Despite no further chest pain, no evolution of ECG findings, and three serial negative troponins, the ED team was concerned for Wellens. 

3 serial negative troponins should suffice in a case like this to rule out ACS.

However, the providers advised the patient that he should be admitted for further risk stratification. The patient declined and signed out against medical advice.


Learning Points:

There are many causes and patterns of T-wave inversion. And among them, many can mimic Wellens pattern (which is simply anterior reperfusion T wave inversion). There are some clinical features that help distinguish them, and expert ECG interpretation can help a great deal to distinguish them. Bottom line: see a bunch of them, follow up the results, and compare them to the cases we've posted - you will become great at it.

Normal variant patterns can change over time.

True reperfusion T wave inversions must evolve over time (must either progress through the reperfusion sequence of deepening T wave inversions, or resolve due to very brief reversible ischemia, or reocclude!). If any T wave inversion pattern does not evolve at all over serial ECGs, then it is not due to ischemia.

If a patient has reperfusion T waves that are evolving along the reperfusion sequence (becoming full T wave inversion and deeper), then there has been substantial ischemia even though there is some reperfusion, and Dr. Smith and I believe it is almost guaranteed that there will be a rise and fall detected in appropriately timed serial high sensitivity troponins.  

It is possible that this rise and fall in Wellens' might be below the URL; for example: 

Result:  < 6 ng/L  →  12 ng/L → 17 ng/L → 9 ng/L  →  < 6 ng/L 


See these other cases involving Wellens mimics:

A Very Elderly Male with a Fall and no Chest Pain



Comparison post:


More Cases of PseudoWellens:




Is it important to recognize LVH Pseudo-infarction patterns?



Pseudo-Wellens' Syndrome due to Left Ventricular Hypertrophy (LVH)



Tuesday, January 18, 2022

Which ACS had more myocardial damage? The one that meets STEMI criteria, or the one with the 'normal' ECG?

This case comes from Jesse McLaren, with some contribution by Smith.

Dr McLaren (@https://twitter.com/ECGcases), is an Emergency Physician in Toronto with a special interest in emergency cardiology quality improvement and education.  He is an Assistant Professor at the University of Toronto.  

2 Cases

Two patients presented with chest pain. How would you interpret their ECGs, and which had the more myocardial damage?


 

Patient 1: 55yo with 5 days of intermittent chest pain, now constant. Normal vitals. 

Old, baseline, ECG


 
Today's acute ECG:


There is normal sinus rhythm, normal conduction, normal conduction, normal R wave progression and normal voltages. There is concave ST elevation in all three inferior leads meeting STEMI criteria, along with hyperacute T waves and reciprocal ST depression and T wave in inversion in aVL; ST depression and T wave inversion in V1-2 from posterior MI, and ST elevation and hyperacute T waves in V5-6 from lateral MI. 


This is an obvious infero-postero-lateral STEMI (+) OMI, identified by the machine and recognized by the emergency physician. The patient was treated with dual antiplatelets, heparin and nitro, and the cath lab was activated. 

 

Two minutes later the chest pain resolved and the ECG was repeated: 


This ECG, if it had been recorded in isolation, would be highly suspicious for acute ischemia, but not OMI

There is resolution of the inferolateral ST elevation but residual reciprocal ST depression in aVL, and mild precordial ST depression. 

Despite having a transient Occlusion, with ST segments that meet STEMI criteria, the patient was still sent to the cath lab, and before the procedure had another episode of chest pain with recurrence of infero-postero-lateral STEMI(+)OMI ECG:


On angiogram there was a 99% circumflex occlusion, but with TIMI-3 flow, which was stented. All troponins were completely normal, at 2 ng/L, just above the limit of detection (LoD).   (Abbott Alinity high sensitivity troponin assay, LoD = 1.6 ng/L; URL = 26 ng/L for men, 16 ng/L for women).   

Notice that we never called this a "STEMI" because it never actually met the definition of acute MI!!

The definition of MI requires at least one elevated troponin, so the patient actually "ruled out" for acute MI!

  

Post cath ECG:


Returned to baseline, without Q waves or reperfusion T wave inversion. 

By itself, this would be a non-diagnostic ECG.  

Discharge diagnosis: "STEMI" (technically NOT)

Imagine if that first ECG had never been recorded.  This patient could have been sent home, then re-infarcted at home and died.

Unstable Angina Still Exists!!
Unstable Angina may have transient ST Elevation


 


Patient 2: 65yo with 30 minutes of chest pain and normal vitals. Old then new ECG:


 

There is normal sinus rhythm, with 1st degree AV block and otherwise normal conduction, normal axis, normal R wave progression, normal voltages. 

 

Compared to prior there is subtle concave inferior ST elevation which does not meet STEMI criteria. But there are also inferior hyperacute T waves (large relative to the QRS complex and compared to baseline), and there is new primary reciprocal ST depression and T wave inversion in aVL, which is highly sensitive for inferior OMI. There may also be some pseudonormalization of the ST segment in V2 from posterior MI.


Despite being STEMI negative and labeled normal by the machine, the physician was concerned so gave aspirin and the ECG was repeated 20 minutes after the first:


 

ECG is similar and patient had ongoing pain. Treated with dual antiplatelets, heparin and cath lab activation: 100% mid RCA occlusion. First trop 26 (borderline normal) and peak 55,000, with inferior basal hypokinesis. 

A peak troponin I of 55,000 ng/L is a level that is associated with very large acute MI (lots of myocardial loss).

Discharge ECG: 


Inferior QS waves and reperfusion T wave inversion, with reciprocal large T wave in aVL; and large T wave in V2-3 reciprocal to posterior reperfusion T wave inversion. 

 

Discussion

 

According to the current paradigm based on ECG millimeter criteria, the first patient had STEMI  requiring emergent reperfusion while the second did not have STEMI so could have been treated with delayed reperfusion. But the second patient had a totally occluded artery leading to a large MI despite rapid reperfusion, and admitting them as “NSTEMI” with next day angiography could have been fatal. According to the discharge summaries, which seemed to be based on culprit lesions that received rapid reperfusion, both patients had “STEMI” despite the first never having a rise in troponin and the second not meeting STEMI criteria.

 

We need to start with the underlying pathology. Both patients presented to the ED with Occlusion MI, i.e. “acute occlusion or near occlusion of a major epicardial coronary vessel with insufficient collateral circulation, resulting in imminent necrosis of downstream myocardium without emergent reperfusion.” Both patients also had ECGs diagnostic of OMI on ED presentation: rather than falsely separating these ECGs into STEMI vs NSTEMI based on ST elevation millimeter criteria, we can see that they both had some degree of inferior ST elevation along with hyperacute T waves and reciprocal change in aVL. Both STEMI(+)OMI and STEMI(-)OMI have similar clinical, laboratory and echocardiographic features.


These cases had different outcomes, not based on which met STEMI criteria, but based on which OMI had rapid reperfusion. 


The first patient presented with STEMI(+)OMI but had such rapid spontaneous reperfusion, followed by angiography, that they avoided myocardial necrosis completely—without a rise in troponin or ECG evidence of infarction or reperfusion. (But if this “transient STEMI” had not had rapid cath lab activation, they might have re-occluded and developed a preventable infarct).   


In fact, this case does not even meet the formal definition of myocardial infarction (!), by the 4th Universal Definition, which requires a rise and fall of troponin with one value above the 99th percentiile.  It is, in fact, ST Elevation Unstable Angina.  Had the patient had ECGs recorded at different moments, this would have been entirely missed 


The second patient presented with STEMI(-)OMI but had a total occlusion that persisted despite initial management and was only relieved in the cath lab—with a resulting significant rise in troponin despite rapid diagnosis, and ECG evidence of infarction and reperfusion. Instead of these patients both having a discharge diagnosis of “STEMI”, the first had unstable angina from “OMI that is so brief or so quickly treated that troponins do not rise, MI prevented”, while the second had STEMI(-)OMI.

 


 

Take home

1.     Automated interpretation is unreliable, even those labeled “normal”

2.     STEMI criteria has poor sensitivity for Occlusion MI

3.     Primary reciprocal ST depression in aVL is highly sensitive for inferior OMI, and can highlight subtle inferior ST elevation and hyperacute T waves 

4.     Acute coronary occlusion is a dynamic process that can spontaneously reperfuse and reocclude, and "transient STEMIs" are at risk for reocclusion

5.     Initial troponins are unreliable for STEMI/OMI, and serial troponins can miss unstable angina from transient occlusions

6.     MIs should be classified based on the underlying pathology of OMI/NOMI, not STEMI/NSTEMI criteria, and this should be reflected in the discharge diagnosis to accurately track and learn from cases

 

References

1.     Bischof et al. ST depression in aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J Emerg Med 2016

2.     Meyers et al. Comparison of the ST-elevation myocardial infarction (STEMI) vs NSTEMI and Occlusion MI (OMI) vs NOMI paradigms of acute MI. J of Emerg Med 2021


 

Sunday, January 16, 2022

Acute respiratory distress: Correct interpretation of the initial and serial ECG findings, with aggressive management, might have saved his life.

 Written by Pendell Meyers with edits by Smith


NOTE: Please check out My Comment at the very bottom of this post — in which I amplify discussion by Drs. Meyers & Smith on some subtle-but-important ECG findings on the initial ECG Ken Grauer, MD —


A man in his 60s called EMS apparently for shortness of breath. EMS found him in distress and hypoxemic requiring 4 L nasal cannula to maintain oxygen saturation greater than 93%.

Here is his triage ECG:

What do you think?




An old ECG was available on file, from 2 years ago:

RBBB, otherwise normal.




The triage ECG is diagnostic of life threatening hyperkalemia (sodium channel blockade would also produce this pattern, but the patient was not known to be on any sodium blocking medications). There is the very common brugada pattern STEMI mimic seen in V1 and partially in V3 and aVR. There is also STE in III with reciprocal STD in I and aVL which is due to the hyperkalemia.

When hyperkalemia causes STEMI mimics, in my experience, the most common areas where the false positive STE morphology is located are, in this order: right precordial leads (due to brugada morphology), inferior leads (as seen here), and then the high lateral leads. We have many such cases on the blog, see links below. 

This ECG is easy for those who have been taught this hyperkalemia pattern, and almost impossible to understand for those who haven't. 

Unfortunately, the providers interpreted this ECG as a "STEMI" and activated the cath lab. The interventionalist called the ED provider and completely agreed that the ECG represented STEMI. However, they informed the ED team that the patient's size was not physically compatible with the cath lab table, and thus could not be cathed. Instead, the interventionalist recommended thrombolytics.

Tenecteplase was given immediately. 

At this time, the patient was still in respiratory distress; he was placed on noninvasive positive pressure ventilation, with intact mental status.

Soon afterwards, the initial labs returned:

K 8.3 mEq/L

Na 125 mEq/L

Creatinine 9.41 mg/dL

High sensitivity troponin I returned at 6 ng/L (99% URL for men less than 20 ng/L)


The patient was given 10 mg albuterol nebulized, 2 gm calcium gluconate IV, 10 U regular insulin, D50, and 50 mEq sodium bicarbonate.


Meyers comment: this is all reasonable initial therapy, except that 2 gm calcium gluconate will not be enough. Remember that a "normal" initial dose of CaCl is 1 gm, which contains the same amount of elemental calcium as 3 gm of calcium gluconate. You must immediately reevaluate the QRS width and overall morphology and administer more and more calcium until you titrate to normal QRS and absence of dramatic brugada morphology. See cases below where we needed huge amounts of calcium every 20 minutes to keep the patient out of arrest and with a reasonable QRS, up to a total of as much as 24 g of calcium gluconate (or 8 g of CaCl), and more is NOT contraindicated, if necessary.  


Transfer was initiated to the tertiary care center with cardiology, nephrology, and ICU services.

He required constant noninvasive positive pressure ventilation for respiratory support.

Low dose norepinephrine was added for hypotension.

Just before transport to tertiary care facility, around 2 hours after initial presentation, the potassium was re-measured at 8.4 mEq/L.

Then the patient received another dose of albuterol 10 mg, Ca gluconate 2 gm, insulin 10 U, and sodium bicarbonate 50 mEq soon after that measurement, before transport.


He arrived at the ICU and had another ECG recorded:

No significant change, thus no significant progress.

Potassium was re-measured at 8.4 mEq/L. The second troponin returned at 17 ng/L (same assay as above).

Again given: Ca gluc 2gm, regular insulin 5U, and sodium zirconium cyclosilicate 10 gm are given.

2 hours later, the ECG was almost exactly the same, with no progress made.

Before a dialysis catheter could be placed, the patient had deterioration in mental status and required intubation. He experienced peri-intubation cardiac arrest and could not be resuscitated.


Learning Points:

The difference between OMI and hyperK can be deadly. In other words, memorizing the patterns of OMI and hyperK mimics can potentially save lives and prevent false positive administration of thrombolytics or cath lab activation. 

The onus is on Emergency Medicine to be the ones who master the ECG, because we see all the emergent, undifferentiated patients with ACS symptoms, from whom we must recognize the "needles in the haystack" who have OMI, hyperkalemia, and differentiate them from benign chest pain and dyspnea, and all sorts of OMI mimics. At least in the US model, the cardiologist does not see these other patients, and cannot possibly have as much experience with OMI mimics as Emergency Medicine. 

Brugada pattern STE is (I believe) the most common OMI mimic caused by hyperkalemia. Inferior leads and high lateral leads have also been described as in cases below.   The typical hyperK mimic of OMI has a large R-wave, with STE, in V1, V2, and aVR, with a wide QRS, along with a variety of other findings.

In addition to peaked T waves, hyperkalemia causes what I call the "killer B's" of hyperkalemia: Broad (QRS widening), Brady (bradycardias of all varieties), Blocks (AV blocks, bundle branch blocks), Brugada (pattern), and Bizarre (bizarre morphology, sine wave, etc.).

There is no maximum dose of calcium when the patient is at risk of death from severe hyperkalemia.   From my observation of many providers who are not experienced with deadly hyperkalemia, the administration of calcium is often a simple question of "yes or no" or a "checkbox." It is not enough to administer a dose of calcium and wait until the next chemistry panel results. You must titrate the calcium until you have achieved a narrow QRS with an absence of brugada morphology or other dramatic hyperkalemic findings.


Cases of hyperkalemia mimicking OMI:

"Steve, what do you think of this ECG in this Cardiac Arrest Patient?"









































General hyperkalemia cases:

A 50s year old man with lightheadedness and bradycardia


Patient with Dyspnea. You are handed a triage ECG interpreted as "normal" by the computer. (Physician also reads it as normal)







Is this just right bundle branch block?



A 60-something who has non-specific generalized malaise and is ill appearing.


HyperKalemia with Cardiac Arrest. 


Peaked T waves: Hyperacute (STEMI) vs. Early Repolarizaton vs. Hyperkalemia


What will you do for this altered and bradycardic patient?


I saw this computer "normal" ECG in a stack of ECGs I was reading


What is the diagnosis?


Found comatose with prehospital ECG showing "bigeminal PVCs" and "Tachycardia at a rate of 156"


An elderly woman found down with bradycardia and hypotension





A Very Wide Complex Tachycardia. What is the Rhythm? Use Lewis Leads!!






I stopped at July 2014, there were countless great posts before that!



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

MY Comment by KEN GRAUER, MD (1/16/2022):

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

Superb ECG Blog post by Drs. Meyers & Smith on some of the life-threatening but less easily recognizable forms of hyperkalemia.

  • WHY are these cases “less recognizable” for potentially life-threatening hyperkalemia?

 


ANSWER: Because we don’t see the very tall, peaked T waves with slender base that we are looking for ...

 


QUESTION: WHY should these cases be more recognizable than they are to emergency care providers?

 


ANSWER: Because in addition to tall, peaked (and pointed) T waves with a narrow base — there are a series of additional ECG findings to look for. For clarity — I’ve labeled the initial ECG in today’s case (Figure-1). Features of life-threatening hyperkalemia that should be evident on this tracing include the following:

  • Brugada phenocopy pattern in lead V1 (as emphasized above by Drs. Meyers and Smith).
  • QRS widening in a pattern that does not resemble any known form of BBB.
  • Either extremely tiny P waves (vertical BLUE lines in the long lead II rhythm strip in Figure-1) — orno P waves at all (ie, sinoventricular rhythm).
  • Subtle-but-real T wave peaking (RED arrows).


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


Comment:

We all know to look for hyperkalemia in patients predisposed to developing this electrolyte disorder (ie, acute or chronic renal failure; severe acidosis; use of potassium-retaining medications; severe trauma, etc.). Recognition is much easier when one of these “predisposing” conditions is present.

  • But almost all of the patients emergency providers see (ie, in-the-field when EMS is called — or in the Emergency Department) are potentially very ill, and therefore potentially “predisposed” to developing hyperkalemia.


So WHAT is the Rhythm in Figure-1?

As a reminder of WHY determination of the cardiac rhythm can be so challenging when there is significant hyperkalemia — I've added Figure-2.

  • In today's case — I fully acknowledge that I do not know for certain what the rhythm in Figure-1 is. I suspect that the vertical BLUE lines that I've drawn under the long lead II rhythm strip indicate placement of tiny P waves with a prolonged PR interval — BUT — it could also be that there are no P waves — in which case this would either be junctional or sinoventricular rhythm.
  • Practically speaking — it does not matter what the rhythm in Figure-1 is — because IF this patient would be promptly treated with Calcium — whatever this rhythm was would most probably rapidly resolve.


Figure-2: Reasons why determining the rhythm with severe hyperkalemia is so challenging.


BOTTOM LINE: I believe the BEST way not to overlook potentially life-threatening hyperkalemia is to: i) Always consider it in the acutely ill patients you see; ii) Look not only for tall, peaked T waves — but ALSO for:

  • Unexpected bradycardia.
  • Small (or absent) P waves. 
  • 1st-degree AV block (often with markedly prolonged PR intervals).
  • Other forms of AV block (that often do not obey the "usual rules” of AV block).
  • QRS widening (especially if QRS morphology is not in a pattern of a known form of BBB).
  • Unexplained marked right axis in the frontal plane.
  • Brugada phenocopy patterns.
  • More subtle forms of T wave peaking (ie, as seen in Figure-1 — in which although small and not pointed — many T waves are surprisingly more “peaked” than you would expect them to be given how small the QRS is, and how otherwise flat the ST segments are).


For MORE on Hyperkalemia:

  • CLICK HERE for review of the "textbook" sequence of ECG findings with hyperkalemia.
  • CLICK HERE — to listen to my 8-minute Audio on Pearls for ECG Recognition of Hyperkalemia.

 


Recommended Resources