Thursday, May 19, 2022

Chest pain, shortness of breath, T wave inversion, and rising troponin in a young healthy runner.

Written by Pendell Meyers, edits by Smith and Grauer


A man in his late 20s with history of asthma presented to the ED with a transient episode of chest pain and shortness of breath after finishing a 4-mile run. He typically runs 4 to 8 miles per day. This episode was unusual to him because he was still "huffing and puffing" about 30 minutes after finishing his strenuous run in the outdoor heat. No mention of whether the patient had cough.

At the time of evaluation in the ED, his symptoms were resolved. His exam stated that his lungs were clear.


Here is his ECG:









Meyers: This ECG shows sinus rhythm, normal QRS with healthy high voltage, and benign T wave inversion pattern in V3-V5. Dr. Smith and I agree that this is a normal variant ECG, in other words, NORMAL, and no further workup should be based on this ECG, but instead only the patient's symptoms and clinical picture. For in-depth description and examples of BTWI, I'll refer you to my other recent post: Understanding this pathognomonic ECG would have greatly benefitted the patient.



The ECG was read as concerning for Wellens (meaning anterior reperfusion pattern).


Initial high sensitivity troponin I = 27 ng/L (URL for men 20 ng/L for this assay).

CT angio negative for PE or other radiographic pathology.  (No D-dimer was ordered)


A repeat troponin returned at 51 ng/L.


He was given aspirin and heparin and transferred to the local cardiac center for further evaluation.



He was diagnosed with mild AKI which resolved.


Ct coronary angiogram showed normal coronary arteries.  


Smith note: I think CT coronary angiogram is reasonable with the elevated troponins and symptoms.  Exercise test would also have been reasonable.  I would always do a peak flow in a patient like this and if not at predicted value, give albuterol and see if it improves.


Next troponins were 28, then 19, then none further measured.


Several more ECGs were obtained during his admission.



All just normal ECGs with BTWI. 


His symptoms of chest pain and shortness of breath were attributed to an asthma exacerbation during exercise.


He was discharged.




Read about "exercise induced cardiac troponin elevations" here. Here are a couple quotes from the article:

"Exercise intensity and duration, together with exercise‐induced high heart rate, have been the most consistent predictors for the exercise‐induced cardiac troponin elevations."

"Exercise‐induced troponin elevations are common after long‐distance running, but occur rarely (9%) after long‐distance walking, supporting the crucial role of high heart rate in this process."

"The benign troponin release pattern is characterized by relatively low peak concentrations that occur within a few hours after exercise and normalize within 24 hours compared with a more prolonged elevation in myocardial infarction or myocarditis."

Dr. Smith note: I wouldn't necessarily consider this ENTIRELY "benign." It is benign compared to acute MI, but it may be that people with such troponin elevations are at higher risk for long term mortality. It may even be that patients with ECGs with this morphology have a higher long term risk. The important point for our purposes is that they do no represent myocardial infarction. Indeed, they have a higher incidence of structural problems.

Potential Adverse Cardiovascular Effects From Excessive Endurance Exercise

Exercise Is Medicine? The Cardiorespiratory Implications of Ultra-marathon


Bjørkavoll‐Bergseth et al. JAHA 2020.

https://www.ahajournals.org/doi/10.1161/JAHA.119.014408

177 participants of a 91-km recreational mountain bike race had pre-race, 3-hour post race, and 24-hour post race evaluations including cTnI and cTnT measurements. Both cTnI and cTnT increased in all individuals, reaching the highest level at 3 hours after the race. Of all heart rate data recorded during the race, the duration of exercise with HR greater than 150 bpm correlated best with the rise in troponin levels.

Median cTnI at baseline was 1.9 (1.6–3.3) ng/L, increased to 60.0 (36.0–99.3) ng/L at 3 hours (P<0.001) and declined at 24 hours to 10.9 (6.1–22.4) ng/L (P<0.001). A similar profile was found for cTnT: baseline, <3.0 (<3.0–3.8) ng/L; 3 hours, 38.3 (25.6–55.2) ng/L (P<0.001); and 24 hours, 11.0 (7.2–17.4) ng/L (P<0.001).


Paana et al. International Journal of Cardiology 2019.

https://www.internationaljournalofcardiology.com/article/S0167-5273(19)32014-5/fulltext

In this study, 40 presumably healthy male marathon runners had their cardiac troponin and other findings measured before and after running a marathon. 39 pts (97.5%) had baseline cTnT values below the reference limit (less than 14 ng/L). 38 pts (95%) of participants had post-marathon cTnT concentration rise above this reference limit. The median post-marathon cTnT was 41 ng/L, and the 95th percentile concentration was 90 ng/L. None reported "cardiac symptoms" after the race.






See this single post for many examples of BTWI:

Understanding this pathognomonic ECG would have greatly benefitted the patient.







===================================
Comment by KEN GRAUER, MD (5/17/2022):
===================================
Concise but important presentation by Dr. Meyers that emphasizes the following points:
  • The History is KEY.
  • BTWI (Benign T-Wave Inversion) Syndromes are often mistaken for more serious pathology.
  • Exercise-Induced Troponin Elevation — is a real entity. As per Dr. Meyers — today’s case was typical of this entity because: i) Troponin elevation occurred in an otherwise healthy adult after an episode of long-distance running; ii) Peak troponin was no more than minimally elevated; andiii) Troponin levels rapidly returned to normal (whereas the troponin elevation of acute MI is generally higher and lasts much longer).

Regarding the History: 
It sounds from the History as if this patient has at least a significant component of EIA (Exercise-Induced Asthma). It also sounds from events described that he was unaware of this possibility. Many variations of asthma exist — including non-exercise-induced — primarily exercise-induced — and/or — some combination of these 2 entities. Clearly, overexertion from excessive hot temperature during this patient's run may have predisposed to precipitating bronchospasm on the day of admission.
  • Attention to the history could help elicit how likely it is that this patient’s symptoms were (or were not) the result of EIA.
  • definitive diagnosis could be made by a combination of history (regarding the circumstances of symptom occurrence, treatments tried, and the course over time of this patient’s asthma) — and — by lung auscultation and/or peak flow measurement (that can be easily taught to the patient) before and after exercise.
  • Effective management of EIA can usually be achieved by patient awareness of this entity — and — with appropriate prophylactic and/or post-exercise bronchodilator use.
  • Referral to the patient’s primary care clinician (added as an essential part of this patient’s hospital discharge instructions) — can facilitate optimal longterm management (and hopefully avoid recurrent ED visits in the future for the same problem).
  • A nice Review of EIA by Molis and Molis can be found in Sports Health 2:311-317, 2010.

Regarding the ECGs in Today’s Case:
While I immediately suspected that the initial ECG in today's case was benign — I thought it somewhat atypical, because T wave inversion is minimal in leads V1,V2 — and much more impressive in leads V3,V4 (See ECG #1 in Figure-1).
  • NOTE #1: There clearly is misplacement of the lead V1 and V2 electrodes (which are placed too high on the chest) — because: i) There is a terminal r’ complex in lead V1 — with an overall QRS morphology that closely resembles the PQRST complex in lead aVR — and, with an all negative P wave in this lead V1; andii) I would not expect the inverted T wave amplitude to decrease from lead V1-to-V2 — and then to increase again from lead V2-to-V3.
  • Please see My Comment at the bottom of the page in the April 17, 2022 post of Dr. Smith's Blog — for concise review on how to quickly recognize too-high placement of the lead V1 and V2 electrodes.
  • Given that the reason for admitting today's patient to the hospital was mainly because his initial ECG was perceived as “abnormal” and possible Wellens' Syndrome — I would have immediately repeated the initial ECG as soon as I recognized the obvious misplacement of the V1,V2 electrodes. Doing so would have immediately produced a repeat tracing similar to ECG #2 — which I feel is even more typical for a BTWI variant with ST elevation (because of a much more logical progression of QRS complexes and ST-T wave appearance as one moves from leads V1-thru-V4).

  • NOTE #2: In support that the lead V1,V2 electrodes in ECG #1 were in fact placed too high — is the appearance of these leads in ECG #2, in which: i) There is no longer any r' component in lead V1; ii) The P wave in lead V1 now has an initial positive component; iii) The rS complex in lead V1 of ECG #2 no longer resembles the Qr complex in lead aVR; andiv) There is now a much more natural R wave progression as one moves from lead V1-to V2- to V3, compared to the less logical R wave progression that there was in ECG #1.

  • NOTE #3: For review of the "many faces" of benign ST-T wave variants — numerous examples are shown and discussed in the March 22, 2022 post by Dr. Meyers — and earlier, in the January 7, 2015 post in Dr. Smith's Blog.

Final Points:
  • We know that the patient in today's case is athletic (he runs 4-8 miles daily!) — but we were not told his race. This is relevant — because many of the benign ST-T wave variants are far more common in young adult, athletic, African-American males. Awareness of this racial predominance may be helpful in estimating the likelihood of a normal variant ECG pattern.

  • Did YOU notice the rhythm in ECG #1? This is not a simple sinus rhythm. In addition to marked variation in the R-R interval throughout the long lead II rhythm strip — there appears to be a change in P wave morphology (ie, the P wave being of much smaller amplitude at the slower rates, before beats #1, 2 and 12 in the long lead II rhythm strip — compared to the larger and notched P wave in front of beats #3-thru-11). This gradual change in P wave morphology as the heart rate varies could be consistent with a wandering atrial pacemaker.
  •  
  • To Emphasize: WAP (Wandering Atrial Pacemaker) is typically a benign variant rhythm that is not important clinically to today's case. That said — My point is to illustrate how EASY it is to overlook non-sinus rhythms if you are not systematic in your approach to ECG interpretation (and if you do not routinely spend an "educated" 3-to-5 seconds looking at regularity and consistency in P wave morphology in the long lead rhythm strip of every ECG you encounter)!

  • Technically — We cannot diagnose WAP with certainty from the 12-beat rhythm strip shown in ECG #1 — because shift between at least 3 different atrial pacemaker sites is needed to satisfy criteria for WAP — and we only see 2 different P wave shapes in the long lead II of ECG #1.
  • In contrast — the difference in P wave morphology is more subtle in ECG #2 (and more difficult to distinguish from the slight variation in sinus P wave morphology that is sometimes normally seen). 
  • NOTE: Please see the Addendum below if interested in more detail regarding the ECG diagnosis of WAP.

Figure-1: I've reproduced the first 2 ECGs in today's case (See text).


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

ADDENDUM: 
I review KEY features of a Wandering Atrial Pacemaker (as opposed to MAT) in the 3:30 minute Audio Pearl below:


 

Figure-2: Written review of wandering atrial pacemaker (from ECG Blog #200 — which illustrates a case).

Saturday, May 14, 2022

A 30-something with palpitations and lightheadedness

A 30-something male without any significant past medical history presented with palpitations and presyncope.

Here is his ED ECG:

Regular Wide Complex Tachycardia at a rate of 229
First: What do you want to do?
Next: What do you think is the ECG diagnosis?









First. Before getting into analysis, a regular wide complex tachycardia could be 

1. ventricular tachycardia (VT) or 

2. AV reciprocating tachycardia (AVRT, antidromic WPW) or 

3. SVT with aberrancy.  (SVT would usually be AVNRT or orthodromic WPW)

Since adenosine is safe in VT, and it works for AVRT and AVNRT, it is worthwhile trying adenosine.  Or, of course, you can always use electrical cardioversion.

Providers gave 6 mg of adenosine with no response, followed by electrical cardioversion.

This is what I texted back: "VT or AVRT. (Antidromic WPW).  I am sure you already shocked it, right?"

Next. ECG analysis: This is a regular wide complex tachycardia.  There are no P-waves.  The QRS onset is very slow. See magnified leads below.  The time from QRS onset to peak is approximately 110 ms.  

This is too long for either AVNRT or for Idiopathic VT.  Briefly, idiopathic VT is VT in an otherwise normal heart and initiates in conducting tissue and therefore has a rapid onset similar to SVT with aberrancy). See this post: Idiopathic Ventricular Tachycardias for the EM Physician.  

Such a slow onset is appropriate for VT in the context of myocardial disease, or for AVRT.

Here I put a lines, or arrows, at the onset (black) and end of the ONSET (blue) of the QRS.  I started in lead II at the bottom, where it is easiest to see the onset.  



The QRS in aVR starts with a 40 ms q-wave (see the dip after the blue arrow).  The onset of the QRS ends at the 2nd peak.  Thus, the QRS from onset to peak (the initial depolarization takes about 110 ms).  
This is prolonged and would not be so slow if it were through conducting tissue, as it would be with AVNRT or with idiopathic VT.


Here is the post cardioversion ECG (texted to me):

This what I texted back: "Could be WPW. You don’t always see Delta waves."


After cardioversion, echo showed excellent LV function.


Final analysis:

1. Good LV function means that if this is VT it would likely be idiopathic VT

2. But idiopathic VT should have a rapid onset

3. This has a slow onset, so it is unlikely to be either type of VT.

4. Finally, Right ventricular outflow tract VT, which responds to adenosine, has an LBBB morphology and inferior axis, which is not present here.

5.  Therefore AVRT is most likely, even though there are no delta waves.

This was the note of our electrophysiologist:

“… Although the morphology is consistent with ventricular tachycardia, we cannot completely rule out antidromic AVRT originating from LV base insertion site of an accessory pathway.  The EKG during sinus rhythm does not show robust preexcitation, but we will keep in mind that for left-sided accessory pathways may not show robust preexcitation during sinus rhythm since this is essentially dependent upon relative conduction of the AV node versus accessory pathway (if any).”

Outcome

Electrophysiologic study showed an accessory pathway (WPW, antidromic AVRT)

Why did adenosine not work?  6 mg often does not work, but especially in low flow states.  Our electrophysiologist, Rehan Karim, explains: "At this HR in general one might expect overall transit time for any IV drug to be very slow to reach the heart. Adenosine as you know has very short half life so a small dose like this probably would fade away before it would reach the target area."

Dr. Karim wrote some further key take away points are:

1. Degree of pre-excitation (“WPW”) during sinus rhythm is dependent on competition between the AV node and pathway - and is also impacted by relative location of pathway. If I live in West Suburbs of Twin Cities, I’ll probably take I-35 W rather than I-35 E unless it is blocked for whatever reason.

So if you don’t see pre-excitation during sinus rhythm, it doesn’t mean there can’t be any - as sinus node is right atrial structure and left sided pathways may not show robust pre-excitation if someone has fast conducting AV node!

2. Antidromic AVRT morphologically will meet the criteria for “VT” originating from “insertion site” of the accessory pathway- because essentially that’s where Ventricular activation is originating. Now it can NEVER have negative concordance though - because the accessory pathways usually insert at base of the heart rather than apex!




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

MY Comment by KEN GRAUER, MD (5/14/2022):

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


What I liked most about today's case — was the skillful use of bedside Echo in the ED by Dr. Smith to facilitate rhythm diagnosis! I'd add the following comments to his excellent clinical decision-making strategy.
  • As per Dr. Smith — the initial rhythm in today's case is a regular WCT ( = Wide-Complex Tachycardia) a~230/minutewithout clear sign of atrial activity. Dr. Smith suggested the following Differential Diagnosis for this WCT rhythm: i) VT; ii) Antidromic AVRT (in a patient with WPW)and/oriii) SVT with aberrant conduction.

  • I'd add: iv) SVT with preexisting BBB (Bundle Branch Block) to the above differential diagnosis — as instead of an initially narrow QRS complex (that manifests aberrant conduction as a result of the rapid rate) — the etiology of this regular WCT rhythm could be an SVT in which the QRS was already widened (ie, "preexisting" BBB).

  • Dr. Smith narrowed the likely differential for aberrantly-conducted SVT to either AVNRT or orthodromic AVRT. This is because the ventricular rate of ~230/minute for today's tracing is too fast for sinus tachycardia in an adult — it is slower-than-would-be-expected for 1:1 AFlutter — and — faster-than-would-be-expected for 2:1 AFlutter. While Atrial Tachycardia could be possible at this rate — ATach is far less common in practice than either of the reentry SVT rhythms (which are AVNRT and AVRT).

  • Dr. Smith highlighted delay in the initial conduction time (perhaps seen best in the slow upslope for the R wave in leads V1-thru-V4 — as well as measured in Dr. Smith's magnified view of lead aVR that is shown above). This delay in initial conduction of the QRS makes it much less likely that a supraventricular mechanism is operative (since initial conduction with AVNRT and orthodromic AVRT is usually fast, being transmitted over the normal AV nodal pathway).

At this point — the patient was electrically cardioverted, and a post-cardioversion Echo in sinus rhythm showing normal LV function was obtained.
  • PEARL #1: Getting an Echo when your arrhythmia patient is stable can sometimes prove highly insightful for determining the rhythm. For example, in today's case — Knowing that the Echo obtained after conversion to sinus rhythm revealed normal LV function — allowed Dr. Smith to deduce that ischemic VT was unlikely (since this entity is almost always associated with at least some impairment of LV function)
  • Use of Echo therefore narrowed diagnostic considerations for today's rhythm to 2 entities: i) Antidromic AVRT (in a patient with WPW) — vs — ii) Idiopathic VT (ie, that group of ~10% of all VTs that occurs in patients who do not have underlying heart disease).

PEARL #2: I favor addition of QRS morphology features in my considerations to enhance prediction of the rhythm etiology.
  • While exceptions exist — supraventricular conduction with QRS widening (ie, from either aberrancy — or from preexisting bundle branch block)tends to resemble some form of conduct defect (ie, either RBBB, LBBB, or RBBB with LAHB or LPHB)QRS morphology in today's initial tracing does not resemble any known form of conduction defect because: i) The uniformly amorphous and slurred complexes in leads V1-thru-V4 are completely lacking in the triphasic appearance that RBBB typically shows in lead V1 — and — lacking in the usual progression of an RBBB pattern as one moves across other anterior leads; andii) The multiphasic (fragmented) and virtually isoelectric complex in lead III is not consistent with any known hemiblock pattern.

  • QRS morphology in today's initial tracing is not consistent with either of the 2 most common forms of idiopathic VT — which are RVOT VT (Right Ventricular Outflow Track VT) and Fascicular VT. I've reproduced the summarizing Table from my discussion of this topic in the February 14, 2022 post in Dr. Smith's Blog in Figure-1. Today's initial tracing is not RVOT VT — because it does not have an LBBB-like appearance in the chest leads. This initial tracing is also unlike Fascicular VT because it is too wide, too amorphous in its anterior lead shape, and too fragmented and isoelectric in lead III. While a small percentage of the idiopathic VTs manifest a less recognizable QRS morphology — the initial delay in conduction (as per Dr. Smith), marked QRS widening, and other morphologic features described above make idiopathic VT highly unlikely as the diagnosis.

  • In contrast — the very rapid rate of today's reguar WCT rhythm — in association with the initial slurring of the wide positive complexes in most chest leads would seem perfectly consistent with antidromic AVRT.

BOTTOM Line Regarding Today's CASE: 
Determining the precise etiology of today's initial tracing is not needed for appropriate initial management. As Dr. Smith said in his initial comment, "I am sure you already shocked this rhythm, right?" While brief trial of medical therapy (ie, with use of Adenosine) may be reasonable if the patient is hemodynamically stable — the chances are high that electrical cardioversion will soon be needed.
  • PEARL #3: It is not always possible to distinguish between VT vs antidromic AVRT from an initial ECG showing a regular WCT rhythm. Statistically — over 95% of such rhythms will turn out to be VT. Clinically — this distinction is not essential, since appropriate initial management considerations are usually similar (ie, both rhythms will respond to electrical cardioversion).

  • That said — today's case is insightful for illustrating how use of Echo and assessment of QRS morphology may guide diagnostic considerations. Knowing that the probable etiology of the very rapid WCT in today's case is antidromic AVRT can help expedite definitive therapy — which will be EP referral for ablation of the patient's "culprit" accessory pathway.


Figure-1: Review of KEY features regarding Idiopathic VT (CLICK HERE — for the source of this Summary).






Wednesday, May 11, 2022

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?

 Written by Pendell Meyers, additions and edits by Grauer, Smith, McLaren


Below we have 5 cases of adults (ranging from 40-70 years old) who all presented to the ED with acute nontraumatic chest pain that sounded at least somewhat like potential ACS to the provider. 

You should look at each ECG and decide if it is OMI, not OMI, or something else.

Our goal in this post is to compare and contrast OMIs with false positives that mimic them. In this post we will examine the anterolateral distribution that has been described as the "South African Flag Sign." (SAFS)

It is very hard to describe why an ECG expert can easily differentiate these 5 cases. Some of these cases will appear to violate some rules of thumb that are commonly given in rudimentary ECG education. In the end, what matters is accuracy - can you tell which are "real" and which are "fake"? For now, the only thing that can tell the difference is expert human interpretation by someone who has spent much time to memorize these ECG patterns and correlate them with patient outcomes.

Think about faces: you can recognize your friend instantly.  But can you describe why?  Did you measure her nose?  The size of her eyes?  No.  An EKG is like a face and you need to get to know them so you can recognize them.  This is what we hope to teach to artificial intelligence. 

A short discussion of the SAFS pattern will come at the end for review.


Case 1


 - this case had a prior ECG available, here:



Case 2



Case 3



Case 4



Case 5




Scroll down for answer key and discussion.



















Case 1 - Normal variant (Not OMI, False Positive STEMI criteria)

With no clinical information at all, I sent this to Dr. Smith who immediately said "Not OMI." I responded: "Correct. But you can see why well meaning learners who are trying to learn to find hyperacute T waves and the south african flag sign are so upset when I told them that!"

ECG: Sinus rhythm. QRS grossly within normal limits. STE in I and aVL and V2, reciprocal STD in III and aVF. The T waves are tall in I and aVL, but not "fat." They are not hyperacute, because they are not "inflated with air" in my opinion. The morphology of the STD and TWI in III is especially specific for NOT OMI, and it has the appearance of LVH with "strain pattern." It is fake, not OMI.


Clinical info: 40s year old woman presented to the ED for off and on chest pain over a week or so, with an episode today that woke her from sleep and wouldn't go away. There was associated cocaine use, but unclear if recently.

Here is an example of a prior ECG on file:


STEMI was activated. Cardiology refused and cancelled the cath lab activation, reportedly stating that they believed that her ECG findings were consistent with prior episodes of cocaine use. I am not quite sure what that means or what exactly their reasoning was, but regardless no angiogram happened.


The patient was admitted to medicine for high risk chest pain.

Three serial troponin I measurements were each 9 ng/L.

Potassium level was 4.1 mEq/L.

She checked out against medical advice before any further workup was done.



Case 2 - D1 OMI (STEMI[-] OMI)


ECG: Sinus rhythm, QRS grossly normal. Subtle STE in I and aVL, with tiny terminal T wave inversion in aVL. Reciprocal STD in II, III, aVF. V2 has the slightest suggestion of STE with convex ST segment. This one matches many prior cases of true SAFS in my experience, and the morphology looks like acute OMI at least affecting the high lateral leads. The slight terminal TWI in aVL may suggest that it is starting to reperfuse.


Clinical info: 70s year old M with chest pain for 1 hour. 

Initial high sensitivity troponin I = 27 ng/L (below the URL; i.e. normal)

Given ASA, morphine, NTG for ongoing pain.

Repeat trop 233, then 14,000, then greater than 25,000 ng/L

As this was not recognized as OMI, cath was done too late and showed 100% thrombotic acute D1 occlusion, stented. 

EF 35%, WMA mid-apical anterior, lateral, and apical myocardium.

Post PCI ECG:




Case 3 - D1 OMI (STEMI[-] OMI)


Sent to Dr. Smith with no information at all, who immediately responded with: "This one is OMI."

ECG: Sinus rhythm. QRS grossly within normal limits. Similar to case above with STE in I and aVL with reciprocal STD in III and aVF. Similar V2 as case above. This time the T waves are upright in I and aVL. Leads III and aVF have a very concerning "down-up" morphology that is specific for reciprocal STD from OMI in lead aVL. 


Clinical info: 50s year old man with tobacco use presents for acute substernal chest pain just prior to arrival.

Initial troponin less than 6 ng/L (less than limit of detection).

Repeat troponin 17 ng/L.

Echo shows hypokinesis of the anterolateral myocardium.

Repeat trops: 2740, 5835, 7077 ng/L. None further ordered.

Cath shows acute thrombotic occlusion of D1, deemed small and not suitable for PCI. 

No further ECGs recorded.

Note: the first 2 troponins were negative; if you rely on troponin to make this difficult diagnosis, you will lose a lot of time and all of the myocardium at risk!



Case 4 - Normal variant (Not OMI, False Positive STEMI criteria)

Sent with no information to Dr. Smith, who said "Not OMI."


ECG: Sinus rhythm. QRS shows relatively high voltage, but maybe not meeting clear LVH criteria. Could also be simply healthy young high voltage. There is STE in I, aVL, and V2, with convex ST segments and reciprocal STD in II, III, aVF with TWI. I strongly suspect these T waves are not hyperacute (unless a baseline ECG later proves me wrong), but instead a confusing baseline variant. There is also terminal T wave inversion in V3-V6, which reminds me somewhat of benign T wave inversion pattern (another normal variant). This ECG simply does not look like OMI in my experience.  

See here for many examples of "benign T-wave inversion", just like what you see here in V3-V6


Clinical info: A 50s year old man presented with acute chest pain of several hours duration. 

Two ED troponins were less than 6 ng/L.

Many prior ECGs on file over years, including this one:

No other dangerous cause of chest pain was found. He was discharged.




Case 5 - mid LAD OMI (the easiest one of all 5, but still STEMI[-] OMI)


ECG: Sinus rhythm. QRS grossly within normal except poor R wave progression and left axis (possibly could describe as LAFB). Hyperacute T waves in I and aVL and V2, STE in aVL and V2. Reciprocal STD in II, III, aVF (from high lateral OMI) and STD in V3-V6 (appears to become maximal in V6, likely indicative of a component of subendcardial ischemia). Terminal QRS distortion in aVL. This one is OMI.


Clinical info: 50s year old man presents with chest pain waking him from sleep 6 hours ago.

STEMI activated, at cath lab: total mid LAD occlusion, stented.

First trop 12,960 ng/L, none further measured.

Post cath ECGs:




South African Flag Sign:

This is a particular ECG pattern found in OMI cases affecting the anteroseptal / anterior / high lateral walls. It has been described as a territory corresponding often to the first diagonal artery, but of course there is substantial coronary variation and any artery in the anterior and or lateral areas can cause this pattern. See the diagrams above from Littmann et al. (referenced below) for the visual explanation of why the pattern of ECG changes can be remembered using the image of the South African flag.

Here is a diagram by Ken Grauer of the South African Flag sign, from this prior post:






References:

Durant E, Singh A. Acute first diagonal artery occlusion: a characteristic pattern of ST elevation in noncontiguous leads. Am J Emerg Med. 2015; 33:1326.e3-5

Littmann L. South African flag sign: a teaching tool for easier ECG recognition of high lateral infarct. Am J Emerg Med. 2015; 34.

DOI: https://doi.org/10.1016/j.ajem.2015.10.022



Images from google search.




Learning Points:

If you use the STEMI criteria to decide which patients need emergent reperfusion, YOU WOULD GET ALL 5 OF THESE CASES WRONG. You would falsely activate the cath lab for 2 patients, and withhold treatment of OMI in the other 3!

It can be difficult to determine OMI from OMI mimics, but this is possible with experience and practice, in which you learn based on memorizing the patterns that correlate with the proven outcomes of OMI.

Expertise can correctly overrule many ECg "rules of thumb." Some of the OMIs above have concave ST segments, and some of the false positive ones have convex ST segments! Many of the false positive cases above indeed have reciprocal findings in inferior leads. Reciprocal findings occur regardless of the reason for focal primary findings. If you learn by seeing many cases and their outcomes, you can see which are true positives and false positives.

The South African Flag sign is a nice teaching tool for the anterolateral OMI distribution.




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MY Comment by KEN GRAUER, MD (5/11/2022):

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As I worked through the 5 tracings selected for today's "Quiz Post" by Dr. Meyers — I found myself asking, "What is it about each case?" — that makes me favor OMI or not favor OMI?

  • As per Dr. Meyers — "It is very hard to describe why an ECG expert can differentiate these 5 cases". Words on paper do not suffice — since "the rules" are not always followed.
  • Instead — there is an intuitive (unspoken) form of "pattern recognition" that just "happens" — in the same way that an experienced clinician can look at a patient, and in a matter of seconds know the likely diagnosis.
  • Clearly — seeing the patient and knowing the history would help in your interpretation of these ECGs. But Drs. Meyers and Smith instantly arrived at the correct interpretation in each case without the benefit of any history.

MY Approach:
  • As I contemplated each of these 5 cases without the benefit of any history — I found myself looking for 1 or 2 leads that I knew were either not normal — OR — that I really thought looked like a benign repolarization change.
  • Then I looked for neighboring (or reciprocal) leads that supported that impression.

  • NOTE: The South African Flag Pattern described below by Dr. Meyers adds to the challenge (For more on this pattern — See My Comment at the bottom of the page in the April 8, 2022 post of Dr. Smith's Blog). This is because acute occlusion of the 1st or 2nd Diagonal Branch of the LAD will typically only result in ST elevation in 1 chest lead ( = lead V2) — so you lose the potential benefit of seeing similar abnormal ST elevation in neighboring anterior leads.

I picked 2 of the 5 Cases to comment on. For clarity — I've put these 2 tracings together in Figure-1 — and have labeled the findings that I focused on.

Figure-1: I've reproduced Case #2 and Case #3 from today's post.


What Is It About these 2 Cases?
Beginning with Case #2 — the rhythm is sinus with a PAC.
  • The lead in Case #2 that caught my eye — was lead aVL. The shape of the subtle-but-real ST elevation in this lead is not normal. Adding to my concern is the small q wave, and hint of beginning T wave inversion. This is not the appearance of a repolarization change.
  • In view of the abnormal appearance in lead aVL — the subtle ST elevation in lead I (above the dotted RED line in this lead) suggests a similar ongoing process in this other high-lateral lead.
  • Confirmation that the lead aVL appearance is likely to be acute — is forthcoming from reciprocal changes in all 3 inferior leads (II,III,aVF). The ST segment straightening that we see in these leads (as per the RED lines) — that then leads up into clearly disproportionately tall T waves (considering the modest R wave amplitude) is not normal.
  • Normally — there is slight (1-2 mm) upward concavity ST elevation in leads V2 and V3, that is usually accompanied by an upright T wave. The ST segment coving with slight elevation that we see in lead V2, with hardly any T wave (within the dotted RED rectangle in this lead) — is definitely not a normal appearance for lead V2. Raising suspicion more — is the finding of a QS pattern in both leads V1 and V2.
  • T waves in leads V3-thru-V6 all look disproportionately tall and peaked considering the modest R wave amplitude in each of these leads. Support that this finding is abnormal is forthcoming from straightening of the ST segments (RED lines).

  • BOTTOM LINE: Awareness that acute occlusion (OMI) of the 1st or 2nd Diagonal may cause ST elevation in lead aVL (sometimes also in lead I) — and only in 1 chest lead ( = lead V2) should prompt this diagnosis for Case #2 until proven otherwise. My suspicion that an acute process was ongoing until proven otherwise in this case — was supported by the finding that ST-T waves in no less than 10/12 leads are clearly abnormal! 

What about Case #3?
Once again the rhythm in Case #3 is sinus.
  • Once again — lead V2 caught my eye, as the shape of the subtle-but-real ST elevation in this lead (within the dotted RED rectangle) — is simply not normal.
  • Although a small-but-present initial r wave is seen in leads V1 and V2 of Case #3 — there is no doubt that the ST segment flattening in leads V3-thru-V6 is not normal (especially given the contrast in shape between the subtle ST elevation in lead V2 — and the definite ST straightening in lead V3).
  • As opposed to the shape of the elevated ST segment in lead aVL of Case #2 — I was not initially certain in Case #3 from looking at lead aVL alone, that the ST elevation represented OMI.
  • That said — the 2 limb leads that caught my eye in Case #3, were leads III and aVF. In both of these leads, in addition to ST depression — was a "down-up" terminal T wave which is distinctly abnormal — and which strongly suggested recent (if not acutereciprocal change to the ST elevation in lead aVL.
  • In view of the definitely abnormal ST-T wave appearance of leads III and aVF in Case #3 — the much more subtle-but-present ST segment straightening that we see in lead II completes the inferior lead pattern of "reciprocal changes".
  • Similarly — in view of now knowing that the shape of ST elevation in lead aVL of Case #3 is abnormal — the similar ST-T wave shape in lead I doubtlessly reflects the same ongoing process.

  • BOTTOM LINE: Although the "look" of Case #3 is not quite the same as what we saw in Case #2 (Note especially the reduced T wave amplitudes in multiple leads) — the "theme" of Case #3 is similar. That is — Case #3 manifests ST elevation in leads I, aVL and V2 — ST depression in leads III and aVF, with an acute "down-up" T wave pattern — and in total, no less than 10/12 leads with clearly abnormal ST-T waves. Once again — the diagnosis should be acute OMI of the 1st or 2nd Diagonal until proven otherwise.

What about the Non-OMI Tracings?
I wish I had easy answers for how to quickly recognize the 2 tracings in Dr. Meyers' Quiz that were not OMIs.

  • Here — the History really helps! Even marked ST elevation is often benign when a young adult is either asymptomatic or presents with atypical symptoms. On the other hand — a worrisome history is clear indication of need for more information plus diagnostic testing (ie, stat Echo during chest pain — troponin — repeat ECGs — search for a prior ECG for comparison). IF in doubt — it is best to be prudent until you can rule out an acute event.

The more non-OMI variants that you see — the better you get at recognizing them! There are numerous examples throughout Dr. Smith's ECG Blog.
  • See the April 8, 2017 post — for a nice review by Drs. Smith and Dunbar of some normal variants with T wave inversion.
  • See My Comment at the bottom of the page in the September 11, 2020 post — showing lots of ST elevation in a young adult.
  • The August 22, 2020 post — Even repolarization variants may sometimes show "dynamic" ST-T wave changes.
  • See My Comment in the November 14, 2019 post — regarding distinction between T-QRS-D (Terminal QRS Distortionvs repolarization variants.

  • There are many others — and we continue to post more!

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