Wednesday, December 30, 2020

Chest pain after motor vehicle collision with an abnormal ECG - blunt cardiac injury? OMI? normal variant?

Submitted and written by Morgan Penzler MD, with edits by Pendell Meyers

A man in his early 40s with no significant past medical history was involved in a motor vehicle collision, in which another car struck his driver's side at high speed after running a red light. He was seat-belted, and both side and front airbags deployed. The patient had no symptoms preceding the collision. He required complex extrication from the vehicle by EMS. He was immediately taken to the nearest emergency department, where he had normal vital signs but was complaining of worsening left sided and substernal chest pain. Trauma workup revealed multiple left rib fractures, a small left pneumothorax, a moderate splenic laceration, and some minor pelvic fractures.

The patient reported worsening chest pain, and so an ECG and troponin were ordered.

Here is the initial ECG at 1723:

What do you think? 

Annotated with J points identified in all leads

The ECG shows sinus rhythm with RBBB. The ST segments and T waves are abnormal for RBBB, because there is STE in II, III, aVF, V5 and V6. The STE is concordant in III and aVF. Interestingly, there is no reciprocal STD in aVL. There are large volume T waves in the same leads that are concerning for hyperacute T waves. Overall, this ECG is concerning for lateral and inferior (or apical) OMI. If the RBBB is new, this would be another feature concerning for LAD occlusion (because the LAD supplies the RBB), or blunt cardiac injury in this setting.

Here is a normal (baseline) RBBB for reference:

Initial high sensitivity troponin I returned elevated at 51 ng/L (limit of detection = 6 ng/mL, URL = 12 ng/mL).

Beside echo reportedly showed no clear wall motion abnormalities (I would expect a formal contrast enhanced echo probably should show WMA).

The patient was given aspirin and fentanyl for pain. Given his traumatic injuries, as well as concerning ECG and elevated troponin with concern for blunt cardiac injury, he was transferred immediately to a tertiary care center with both trauma services as well as interventional cardiology.

The second troponin I resulted at 84 ng/L.

Another ECG was recorded at 1759:
I do not see much change. The STE in V4 is slightly greater.

On arrival to the ED at the tertiary care center, the patient complained of ongoing chest pain. An ECG was recorded at that time (1946):

Inferior leads show an obvious STEMI now. There is huge reciprocal STD in aVL now. New STE in V3, and progression of OMI in the lateral leads. STD in V2 would suggest posterior involvement.

Right sided leads were recorded at 2010:
Leads V4-V6 appear to be on the right chest now, and they show only a hint of STE in "V6." I can't be sure, but it appears to me that V3 has not been moved to V3E. In other words, I believe only V4-V6 have been moved to V4R-V6R. Normally, right sided leads should be fully reversed in V1-V6.

The ED team spoke immediately with the interventionalist, and they agreed that the patient should have immediate cardiac catheterization despite the traumatic mechanism and injuries. 

The angiogram revealed a dissection of the mid-LAD (a wraparound LAD) with acute thrombotic occlusion. The RCA was normal. During attempt to open the thrombotic occlusion, the patient suffered a catheter induced dissection of the left main and proximal LAD. The left main, proximal LAD, and mid LAD were all stented, with resultant TIMI 3 flow in all coronaries.

For platelet inhibition (while also in the setting of internal traumatic bleeding), they decided initially on IV cangrelor infusion which can be turned off quickly if need be. The plan was to switch to plavix after traumatic bleeding had been definitively controlled.

The patient was then transferred to interventional radiology for catheter-directed embolization of the splenic laceration.

Repeat troponins were 19,790 and 21,932, then no further troponins were ordered.

The patient had no further significant events during hospitalization and was discharged home on day 5.


Significant cardiac trauma occurs in approximately 10% of patients with severe blunt chest trauma. Isolated coronary artery dissection from blunt trauma is a very rare event. Traumatic dissections are most often seen in the LAD, followed by the RCA and LCX. It is thought that this is due to the relative anterior position of the LAD. 

The ECG is a report from the myocytes of their condition. They do not know the etiology of acute complete ischemia. No matter if its typical ACS, traumatic dissection causing acute occlusion, or spasm, it is the same result to the myocytes, and the same findings can be present on the ECG. 


Allemeersch, G. J., Muylaert, C., & Nieboer, K. (2018). Traumatic Coronary Artery Dissection with Secondary Acute Myocardial Infarction after Blunt Thoracic Trauma. Journal of the Belgian Society of Radiology, 102(1), 4.

James et al.: Dissection of the left main coronary artery after blunt thoracic trauma: Case report and literature review. World Journal of Emergency Surgery 2010 5:21.

Nikparvar, M., Asghari, S. M., & Farshidi, H. (2019). Delayed diagnosis of myocardial infarction in a young man with a blunt chest trauma. Journal of cardiovascular and thoracic research11(3), 251–253. 


  1. Thank you for another great case! What would your algorithm for dealing with a blunt chest trauma patient presenting with chest pain and ST-elevations be? Would you consider CT coronary angiogram if CT is a routine imaging modality for stable trauma patients at a given centre?

    1. I (Meyers) would not consider myself an expert on blunt cardiac trauma. For initial suspicion based on history, I start with ecg, troponin, and cardiac monitoring, which I believe is in line with multiple trauma guidelines for this entity. If the ECG shows clear and diagnostic signs of acute transmural injury (as in OMI, as in the more obvious ecg from this case), then I would immediately involve interventional cardiology for consideration of PCI, because OMI can be either the cause or result (blunt dissection like this case) of an MVC. A diagnostic angio alone has very little harm. If immediate diagnostic angio is not available for a patient like this, I believe they should be transferred to somewhere that has it. Lytics are contraindicated in this case due to significant intraabdominal bleeding. If a cardiologist is in disbelief about the possibility of OMI, and coronary CT angio is available, then it may be very helpful in such a situation to prove or disprove OMI, but would not be my first choice in a case with such an obvious STEMI as seen in repeat ECG above.

      If pt has blunt cardiac injury but no Omi on ECG, then There is usually not an immediate role for angio, and the next step is usually formal cardiac echo and serial trops, and supportive care/monitoring. Let me know what your practice is. Thanks!

  2. Hi Dr. Smith, I have a question about this case:

    Of course leads DII, DIII, V5 and V6 look ischemic, with significant changes compared to the previous one. But, if there is one thing I learned from regularly following your blog, is that you always have to look for reciprocal changes in opposire leads (DI, AvL). In this case, I cannot see any STD in those leads; I can even see slight STE in DI, ando isoelectric ST in aVL. How can we suspect STEMI in this setting? "Only" because inferior leads look "ischemic enough"?
    Plus, V1 shows STD; I remember that one hint of right AMI is STE in that lead. So, how can I even suspect this basing on surface ECG?


    1. We agree that the first ecg is very difficult, with one of the most interesting reasons being the lack of reciprocal STD in aVL. But no single finding is good enough in isolation. Lack of reciprocal findings has never been perfect. Just as two contiguous leads has never been perfect. Ultimately it is very difficult, especially this case. Concordant STE is certainly present, and unless a prior is available it must be considered possibly true until proven otherwise. You prove otherwise just as they did in this case: with serial ECGs and troponins, which confirmed the problem rather than refuted it. We do not propose that this first ecg should be instantly pathognonic for everyone, but there is certainly something to learn in that ecg for everyone. Hope that helps!

  3. truly amazing, very enlightening, and a more than a little frightening. a tightrope to give platelet inhibitor after stenting with a moderate slenic injury.
    thank you Morgan and Pendell.


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