Case submitted by Alex Bracey, Written by Alex Bracey and Pendell Meyers
A man in his 70s complained of acute chest pain followed by witnessed cardiac arrest. He received immediate bystander CPR prior to EMS arrival. EMS found him in VF and administered 4 shocks, multiple doses of epinephrine, and amiodarone with intermittent ROSC, however he was in arrest on arrival to the ED with ongoing CPR via LUCAS device. Overall down time was 35 minutes from the time of arrest to arrival at the ED.
First rhythm check in the ED showed PEA with a wide complex at a rate of approximately 30 bpm. Calcium and epinephine were given at CPR was restarted. He was intubated, and arterial and central venous access were established. The next rhythm check revealed a wide complex rhythm at 78 bpm with a pulse on the arterial line. Norepinephrine was initiated to maintain blood pressure.
An ECG was obtained immediately:
There is a regular wide complex rhythm at a rate of about 85 bpm. The QRS complex is another example of the "shark fin morphology", composed of RBBB and LAFB, with superimposed massive STE in the anterolateral leads.
As you remember from our recent post,
When the QRS is wide, the J-point will hide.
Your next move, of course, is to:
Trace it down and copy it over.
Here is the result:
Meyers comment: Alex sent me this ECG with no clinical information and my immediate response was: "Shark fin! This patient is likely post-ROSC or peri-ROSC, right? LAD occlusion." I then sent it to Dr. Smith who said: "Just another shark fin. Should be obvious."
The cath lab was activated immediately based on this ECG.
iStat labs revealed hypokalemia of 2.2 mEq/L and pH 7.08 (VBG). He was given 300 mg rectal ASA and loaded with 4000U heparin.
Soon after establishing a perfusing rhythm, the patient was gagging and coughing against the endotracheal tube indicating intact brainstem reflexes.
He had recurrent VFib several times requiring defbrillation with ROSC each time. Epinephrine drip was added for additional inotropy.
The cardiology team arrived and another repeat ECG was obtained:
In total, four cardiologists felt that these ECGs "did not represent a STEMI," and they felt that the ECG abnormalities were likely attributable to "hyperkalemia" (until the K returned at 2.2 mEq/L), "metabolic disturbances" and "down time." When the ED physician attempted to show them where the J-point was, highlighting massive anterolateral STE, it was simply not accepted at first in the setting of the wide QRS complex.
The ED attending advocated persistently that the ECG and clinical picture were diagnostic of proximal LAD or even left main occlusion, having seen this pattern several times before on this blog.
Of course, the initial troponin T was undetectable, less than 0.01 ng/mL, which made the ED attending's job even more difficult.
Side note: in our recent study of 467 high risk ACS patients over 6 months, we found 108 with proven OMI. Of those 108, 25% had initial undetectable troponin! The results were even more interesting when stratified by the patient's reported duration of symptoms (see below). Our contemporary troponin T assay does not seem to elevate until at least 3 hours after persistent Occlusion.
After 30 minutes of discussion, another ECG was obtained:
In this ECG the QRS is slightly more organized, and it seems that the ED attending was finally able to convince the cardiologists where the J-point was.
The patient finally went for emergent cath which revealed acute, thrombotic, proximal LAD occlusion (100%, TIMI 0 flow), which was stented with excellent angiographic result. Diffuse CAD otherwise was also noted, but there were no other acute culprits or interventions.
Does angiographic reperfusion guarantee actual downstream reperfusion of the myocardium? No! As we have shown many times including this popular post:
So here is the ECG after reperfusion, decide for yourself whether the actual myocardium is reperfused:
This shows a more organized QRS complex, persistent RBBB but no longer LAFB, and reduced STE in the anterolateral leads with terminal T-wave inversion in aVL, V1-V3, all indicating reperfusion downstream.
Several more serial ECGs were recorded over the next 24 hours which show the progression of reperfusion:
Next morning:
Less than 24 hours after presentation, he was following commands and recognizing his family.
Peak troponin T was 13.06 ng/mL (very large MI). Echo showed EF 30-35%, but views not good enough to assess wall motion abnormalities.
These ECGs clearly have STE meeting the classic STEMI criteria (assuming you interpret the wording of the guidelines to say that the criteria apply in this QRS scenario, which I do but just barely). Thus, this is a STEMI(+) OMI. I personally have been told by more than one cardiologist that scenarios like this do not apply to the STEMI criteria because, similar to their outdated view on LBBB, "you can't tell if there's a STEMI in a QRS like this."
Despite the clearly met STEMI criteria, the diagnosis on the chart and in the cath note is "NSTEMI".
Learning Points:
You absolutely must be able to recognize OMI in the context of wide complex rhythms, because the current STEMI vs. NSTEMI paradigm and current mainstream ECG education has little to offer for such patients.
When the QRS is wide, the J point will hide, so trace it down and copy it over.
Please memorize this "shark fin" STE morphology so that it becomes instantly recognizable, because these are some of the sickest patients who need emergent cath the most. Shark fin is a fusion of QRS and ST elevation, and in some other cases on the blog, although the QRS is wide, the greatest part of the width is ST segment. In this case, most of it was indeed the QRS. Here are other examples:
Massive LAD and or LM occlusion often produces bundle branch blocks, classically RBBB + LAFB or RBBB + LPFB, making the QRS wide and the ST segment deviations more difficult to see.
A man in his 70s complained of acute chest pain followed by witnessed cardiac arrest. He received immediate bystander CPR prior to EMS arrival. EMS found him in VF and administered 4 shocks, multiple doses of epinephrine, and amiodarone with intermittent ROSC, however he was in arrest on arrival to the ED with ongoing CPR via LUCAS device. Overall down time was 35 minutes from the time of arrest to arrival at the ED.
First rhythm check in the ED showed PEA with a wide complex at a rate of approximately 30 bpm. Calcium and epinephine were given at CPR was restarted. He was intubated, and arterial and central venous access were established. The next rhythm check revealed a wide complex rhythm at 78 bpm with a pulse on the arterial line. Norepinephrine was initiated to maintain blood pressure.
An ECG was obtained immediately:
 |
| What do you think? |
There is a regular wide complex rhythm at a rate of about 85 bpm. The QRS complex is another example of the "shark fin morphology", composed of RBBB and LAFB, with superimposed massive STE in the anterolateral leads.
As you remember from our recent post,
When the QRS is wide, the J-point will hide.
Your next move, of course, is to:
Trace it down and copy it over.
Here is the result:
Meyers comment: Alex sent me this ECG with no clinical information and my immediate response was: "Shark fin! This patient is likely post-ROSC or peri-ROSC, right? LAD occlusion." I then sent it to Dr. Smith who said: "Just another shark fin. Should be obvious."
The cath lab was activated immediately based on this ECG.
iStat labs revealed hypokalemia of 2.2 mEq/L and pH 7.08 (VBG). He was given 300 mg rectal ASA and loaded with 4000U heparin.
Soon after establishing a perfusing rhythm, the patient was gagging and coughing against the endotracheal tube indicating intact brainstem reflexes.
He had recurrent VFib several times requiring defbrillation with ROSC each time. Epinephrine drip was added for additional inotropy.
The cardiology team arrived and another repeat ECG was obtained:
 |
| Similar to first ECG. It has been 20 minutes since sustained ROSC, therefore the findings are likely not simply due to low flow during arrest (assuming the patient has had at least several minutes of at least decent coronary perfusion pressure, and this patient had a MAP >65 on low doses of epinephrine and norepinephrine during this time). |
In total, four cardiologists felt that these ECGs "did not represent a STEMI," and they felt that the ECG abnormalities were likely attributable to "hyperkalemia" (until the K returned at 2.2 mEq/L), "metabolic disturbances" and "down time." When the ED physician attempted to show them where the J-point was, highlighting massive anterolateral STE, it was simply not accepted at first in the setting of the wide QRS complex.
The ED attending advocated persistently that the ECG and clinical picture were diagnostic of proximal LAD or even left main occlusion, having seen this pattern several times before on this blog.
Of course, the initial troponin T was undetectable, less than 0.01 ng/mL, which made the ED attending's job even more difficult.
Side note: in our recent study of 467 high risk ACS patients over 6 months, we found 108 with proven OMI. Of those 108, 25% had initial undetectable troponin! The results were even more interesting when stratified by the patient's reported duration of symptoms (see below). Our contemporary troponin T assay does not seem to elevate until at least 3 hours after persistent Occlusion.
 |
| Data presented in abstract form at SAEM and ACEP, in review for publication. |
After 30 minutes of discussion, another ECG was obtained:
The patient finally went for emergent cath which revealed acute, thrombotic, proximal LAD occlusion (100%, TIMI 0 flow), which was stented with excellent angiographic result. Diffuse CAD otherwise was also noted, but there were no other acute culprits or interventions.
Does angiographic reperfusion guarantee actual downstream reperfusion of the myocardium? No! As we have shown many times including this popular post:
Shoulder pain after lifting a heavy box
So here is the ECG after reperfusion, decide for yourself whether the actual myocardium is reperfused:
 |
This shows a more organized QRS complex, persistent RBBB but no longer LAFB, and reduced STE in the anterolateral leads with terminal T-wave inversion in aVL, V1-V3, all indicating reperfusion downstream.
Several more serial ECGs were recorded over the next 24 hours which show the progression of reperfusion:
 |
Next morning:
Less than 24 hours after presentation, he was following commands and recognizing his family.
Peak troponin T was 13.06 ng/mL (very large MI). Echo showed EF 30-35%, but views not good enough to assess wall motion abnormalities.
These ECGs clearly have STE meeting the classic STEMI criteria (assuming you interpret the wording of the guidelines to say that the criteria apply in this QRS scenario, which I do but just barely). Thus, this is a STEMI(+) OMI. I personally have been told by more than one cardiologist that scenarios like this do not apply to the STEMI criteria because, similar to their outdated view on LBBB, "you can't tell if there's a STEMI in a QRS like this."
Despite the clearly met STEMI criteria, the diagnosis on the chart and in the cath note is "NSTEMI".
Learning Points:
You absolutely must be able to recognize OMI in the context of wide complex rhythms, because the current STEMI vs. NSTEMI paradigm and current mainstream ECG education has little to offer for such patients.
When the QRS is wide, the J point will hide, so trace it down and copy it over.
Please memorize this "shark fin" STE morphology so that it becomes instantly recognizable, because these are some of the sickest patients who need emergent cath the most. Shark fin is a fusion of QRS and ST elevation, and in some other cases on the blog, although the QRS is wide, the greatest part of the width is ST segment. In this case, most of it was indeed the QRS. Here are other examples:
"Shark Fin": A Deadly ECG Sign that you Must Know!
Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation
Massive LAD and or LM occlusion often produces bundle branch blocks, classically RBBB + LAFB or RBBB + LPFB, making the QRS wide and the ST segment deviations more difficult to see.
===================================
Comment, by KEN GRAUER, MD (10/4/2019):
===================================
Our THANKS (!) — to Drs. Bracey & Meyers for this important post that illustrates the Shark Fin morphology of acute STEMI with marked QRS widening. Tremendous credit to the team managing this patient for an incredible save! From an ECG perspective — I limit my Comment to an observation about the cardiac rhythm ...
- There are 8 tracings shown on this post. The 2nd tracing shown added vertical lines to indicate location of the J-point — so this 2nd tracing was not a “new” ECG. This means that a total of 7 ECGs were done in this case.
For clarity — the numbering for the ECGs done that I refer to omits the tracing with the vertical lines drawn in to label the J point.
- NOTE: We do not see any P waves until the 5th ECG that was done. I always look for P waves first in lead II — because sinus rhythm is defined by the presence of upright conducting P waves in this lead. My search for P waves next goes to lead V1 (generally the 2nd-best lead for identifying P waves) — and then to the other 10 leads on the tracing. P waves are absent until the 5th ECG ...
- The wide QRS rhythm is fairly regular for the first 3 ECGs that were done.
- The rhythm then becomes irregularly irregular for the 4th ECG that was done — without significant change in the wide QRS morphology.
- Sinus P waves are clearly seen beginning with the 5th ECG. The rhythm is again regular with this 5th ECG — and, this is associated with some narrowing of the QRS complex, with significant change in QRS morphology (ie, less left axis; development of frank Q waves in high lateral and anterior leads, all in association with RBBB).
- A regular sinus rhythm persists for the last 2 ECGs ( = ECGs #6 and #7) — without further change in QRS morphology.
BOTTOM LINE: I’m not sure what the original rhythms were … — but they were not sinus. Shark fin morphology was present — which allowed recognition of acute STEMI despite marked QRS widening.
I wonder what drives cases like this. Sometimes I feel that there is some sort of "consultant bias" coming from a desire to add value, where a consultant is actually less likely to adhere to a diagnosis if they know someone else already made it.
ReplyDeleteThere's also a bayesian problem here: recurrent VF arrest in this age group is overwhelmingly likely to be due to coronary disease. So without clearly non-ischemic etiology, a persistently unstable pt should always get cath.
Finally, I feel troponin adds nothing in these cases. By definition the entire myocardium was not getting perfused. You show very nicely that this is seen too late to affect management in an actual OMI. Conversely, I have seen asthmatics arrest with very high troponin later (why it was ordered, I do not know).
Kind regards,
Maarten Van Hemelen
ID/crit care resident
THANK YOU Maarten for your excellent comments! I’d simply add regarding the issue you raise in your first paragraph about “consultant bias” — my concern that even experienced providers (including a number of cardiologists in this case!) are simply UNAWARE of the entity of “shark fin morphology”. As I mention in My Comment (just above, near the bottom of the page) — recognition of shark fin morphology was made that much MORE challenging in this case, because NO P waves were present until the 5th ECG that was done! As a result, I believe the origin of the cardiac rhythm on these initial tracings was in question. That said — regardless of where the site of origin for the rhythm in initial tracings was — the likelihood of “shark fin” morphology should have been recognized on initial tracings, especially given this 70-ish year old patient’s presentation of new chest pain followed by cardiac arrest! And, as both you and Pendell emphasize — prompt cath WAS indicated. Troponin elevation should not have to be a “deciding factor” in the vast majority of cases. THANKS again for your comment — :)
DeleteThanks Maarten. I agree that recurrent VF and recurrent cardiac instability after ROSC generally deserves emergent cath regardless of EKG. I also agree that troponin should not be the focus of the cath decision, but there are some cases where understanding of OMI is very limited and troponin can indeed become an important part of the decision, see this one: http://hqmeded-ecg.blogspot.com/2019/09/troponin-trajectory-helps-determine.html
ReplyDeleteBut for the vast majority of OMI, I agree: if you're waiting for troponin to make up for your inability to see OMI on EKG, then the benefit of the intervention is likely greatly diminished and you've basically missed the boat. Conversely, you will also have unacceptable false positive cath lab activations if your decision is based on the troponin.