Patient in Single Vehicle Crash: What is this ST Elevation, with Peak Troponin of 6500 ng/L?

A 30-something male was involved in a single vehicle crash and had multiple injuries. 

As a routine part of his critical trauma evaluation, he had an ECG recorded:

There is an rSR" in V1 and V2, with downsloping ST segment and inverted T-wave which is very similar to a Brugada Type 1 phenocopy.   I was shown this ECG and thought that it could perhaps be Brugada, but I was more suspicious for Right Ventricular (RV) myocardial contusion.  The RV is the most anterior part of the chest and is most likely to be contused with anterior chest trauma.  Moreover, this degree of ST Elevation is very unusual for Brugada.

On the other hand, the accident was unexplained.  Did the patient have an episode of VT due to Brugada, and lose consciousness while driving?

Here is one slice of the patient's chest CT

Note the pneumothorax, but the pneumothorax underlies leads V3-V5, not V1 and V2.  

On the other hand, the RV lies directly under leads V1 and V2; this makes pneumothorax less likely as an etiology of the abnormal ECG.

The pneumothorax was expanded with a chest tube

At 17 hours, another ECG was recorded:

It is now much less dramatic and has the morphology of Type 2 Brugada

The hs troponin I peaked at 6500 ng/L -- this strongly suggests myocardial contusion.  Is there also Brugada?

An echocardiogram was done.  Here is the result:

The estimated left ventricular ejection fraction is 50 %.

There is no left ventricular wall motion abnormality identified.

Right ventricular prominence.

Normal right ventricular systolic performance lower limits of normal.

At 40 hours, another ECG was recorded:

Again, it has features of Type 1 Brugada

The electrophysiologist who was consulted was concerned for Brugada:

"It is unclear what precipitated his motor vehicle collision.  The patient is not able to recall events preceding the crash (syncope, dizziness, lightheadedness).  He has a family history concerning for arrhythmia.  Given the circumstances of his car crash, we presume it was due to an underlying arrhythmia.  I suspect his troponin elevation is due to acute myocardial injury (not acute thrombus) related to his polytrauma, possibly cardiac contusion, and reassuring that he has no wall motion abnormalities on TTE."

An MRI was done:  

1) Normal LV function with no wall motion abnormalities
2) Normal dimensions of all cardiac chambers
3) No evidence of left ventricular myocardial scar on delayed enhancement
sequences after contrast administration
4) Hypokinesis involving the free wall of the right ventricle with delayed enhancement, concerning for right ventricular contusion. This appears to be immediately beneath the sternal fracture.   At this point, recommend a short-term follow-up cardiac MRI tailored to evaluation of the right ventricle, in a few days after patient recovery.

2 weeks

Here is the final electrophysiology note:

It is unclear what precipitated his motor vehicle collision.  The patient is not able to recall events preceding the crash (syncope, dizziness, lightheadedness, though reports feeling a popping sound).  He has a family history concerning for arrhythmia with his father requiring some sort of device (PPM, ICD, unclear) at a young age. He has Brugada pattern on EKG with possible syncope, which is concerning for underlying paroxysmal ventricular arrhythmia.  However, his cardiac MRI shows scar that is also possibly associated with his sternal fracture given his location.  

Given the possibility of a ventricular arrhythmia, we would recommend the patient receive a Zoll LifeVest prior to discharge and repeat the cardiac MRI in 2-3 weeks.

Pending the results of the MRI, he could be considered for ICD placement if it does seem more consistent with Brugada syndrome rather than injury to the RV from contusion.  In the meantime will use LifeVest to bridge him during ongoing workup for his RV scar.

Diagnosis: 

1. Definite Right Ventricular Myocardial Contusion and 

2. Possible Underlying Brugada syndrome.

If and when I get a confirmation or refutation of Brugada syndrome, I will update this post.

See our other cases of myocardial contusion and related cases (some of which have an important diagnosis OTHER THAN myocardial contusion!):

You must read this one: A Child with Blunt Trauma -- See how the ECG can be definite for myocardial contusion, but subtle, and what happens if you miss it.   

A man in his 40s with multitrauma from motor vehicle collision

Massive Transfusion for Motorcycle Collision with Hemorrhage, Troponin Elevated.

ECG of pneumopericardium and probable myocardial contusion shows typical pericarditis

Male in 30's, 2 days after Motor Vehicle Collsion, complains of Chest Pain and Dyspnea

Head On Motor Vehicle Collision. ST depression. Myocardial Contusion?

Gunshot wound to the chest with ST Elevation

Would your radiologist make this diagnosis, or should you record an ECG in trauma?

Blunt Trauma in a Child

40-something male in a head-on Motor Vehicle Collision and Splenic Injury

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MY Comment, by KEN GRAUER, MD (11/25/2022):

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

Highly interesting post by Dr. Smith regarding a 30-something male with multiple injuries from a motor vehicle accident. The KEY issues are highlighted by Dr. Smith's title of this post = "What is this ST Elevation, with Peak Troponin of 6500 ng/L?"

When I first saw the initial ECG in today's case — I interpreted the ECG changes in leads V1,V2 as consistent with a Brugada-1 pattern, most likely Brugada Phenocopy. 

• As we've discussed on numerous other posts in Dr. Smith's ECG Blog (See My Comment at the bottom of the page in the May 5, 2022 post) —  a growing number of conditions other than Brugada Syndrome have been found to temporarily produce a Brugada-1 ECG pattern. These include (among others) — acute febrile illness — variations in autonomic tone — hypothermia — ischemia-infarction — malignant arrhythmias — cardiac arrest — and especially Hyperkalemia. Patients with such conditions that may transiently mimic the ECG findings of a Brugada-1 pattern are said to have Brugada Phenocopy. The importance of being aware of this phenomenon of Brugada Phenocopy — is that correction of the underlying condition may result in resolution of the Brugada-1 ECG pattern, with a much better prognosis compared to patients with true Brugada Syndrome.
• 
  
• Kazmi et al have reported on a case in which chest trauma was transiently associated with development of a Brugada-1 ECG pattern (J Am Coll Cardiol 73 [9-Supp-1], 2019). The authors postulate that the mechanism for producing the Brugada-1 ECG pattern was that anterior chest wall trauma caused a non-homogeneous depolarizing current (possibly related to opening of mechanicallly sensitive cardiac K+ATP channels). This ECG abnormality was transient in the case they report — consistent with trauma-induced Brugada Phenocopy.
• 
  
• Alternatively (as per Dr. Smith) — it could be that a malignant arrhythmia that altered consciousness was the precipitating cause of both the motor vehicle crash, and of the Brugada-1 pattern on ECG.

As noted above — Dr. Smith was especially suspicious of RV (Right Ventricular) Myocardial Contusion as primarily responsible for the patient's initial ECG pattern.

• While impossible to rule out a malignant arrhythmia as the cause of the motor vehicle accident — I think it insightful to consider the combination of Brugada-1 Phenocopy + RV Myocardial Contusion as both contributing to the serial ECG changes seen in today's case.

What are the ECG Findings of Cardiac Contusion?

I've copied KEY points from My Comment in the August 6, 2022 post in Dr. Smith's ECG Blog —  regarding the answer to this question. Overall — the ECG is less than optimally sensitive for detecting cardiac injury following blunt trauma. This is because the anterior anatomic position of the RV (Right Ventricle), and its immediate proximity to the sternum — makes the RV much more susceptible to blunt trauma injury than the LV. But because of the much greater electrical mass of the LV — electrical activity (and therefore ECG abnormalities) from the much smaller and thinner RV are more difficult to detect. To REVIEW (Sybrandy et al: Heart 89:485-489, 2003 — Alborzi et al: J The Univ Heart Ctr 11:49-54, 2016 — and Valle-Alonso et al: Rev Med Hosp Gen Méx 81:41-46, 2018) — ECG findings commonly reported in association with Cardiac Contusion include the following:

• None (ie, The ECG may be normal — such that not seeing any ECG abnormalities does not rule out the possibility of cardiac contusion).
• Sinus Tachycardia (common in any trauma patient ...).
• Other Arrhythmias (PACs, PVCs, AFib, Bradycardia and AV conduction disorders — potentially lethal VT/VFib).
• RBBB (as by far the most common conduction defect — owing to the more vulnerable anatomic location of the RV). Fascicular blocks and LBBB are less commonly seen.
• Signs of Myocardial Injury (ie, Q waves, ST elevation and/or depression — with these findings suggesting LV involvement).
• QTc prolongation.
• Brugada Phenocopy (as per the Kazmi et al reference that I cited above).
• 
  
• NOTE: Prediction of cardiac contusion "severity" on the basis of cardiac arrhythmias and ECG findings — is an imperfect science.

Additional KEY Points regarding Cardiac Contusion:

Despite the predominance for RV (rather than LV) injury — use of a right-sided V4R lead has not been shown to be helpful compared to use of a standard 12-lead ECG for detecting ECG abnormalities.

• In addition to ECG abnormalities related to the blunt trauma of cardiac contusion itself — Keep in mind the possibility of other forms of cardiac injury in these patients (ie, valvular injury, aortic dissection, septal rupture) — as well as the possibility of a primary cardiac event (ie, acute MI may have been the cause of an accident that led up to the trauma).
• ECG abnormalities may be delayed — so repeating the ECG if the 1st tracing is normal is appropriate when concerned about severe traumatic injury.
• That said — IF troponin is normal at 4-6 hours and IF the ECG is normal — then the risk of cardiac complications is extremely low.

What About Today's Case?

As I reconsidered today's case — I think the 3 serial ECGs are consistent with both ST elevation in leads V1,V2 from acute RV myocardial contusion + variations of Brugada-1 and Brugada-2 ECG Phenocopy patterns.

• For clarity — I've put together in Figure-1 a visual review of the 2 Brugada ECG patterns (from My Comment in the May 5, 2022 post) — with leads V1,V2,V3 from the 3 ECGs done in today's case. 
• 
  
• In ECG #1 — I still find it hard to distinguish between a Brugada-1 ECG pattern vs ST elevation in leads V1,V2 from acute RV insult vs some combination of the two. I suspect we are seeing a combined ECG effect (as well as a tall, slender R' in lead V1 from myocardial contusion-induced incomplete RBBB).
• 
  
• In ECG #2 — the ST-T wave abnormality is greatly reduced, and now primarily found in lead V2. Although bearing similarity to the Brugada-2 ECG pattern (in Panel B of Figure-1) — the shape of the ST segment descent from the r' peak is unusual for a Brugada-2 pattern in that it includes a short coved segment (outlined in RED — highlighted by the BLUE arrow). Doesn't this shape look to be more consistent with superimposed ST elevation rather than a Brugada-2 pattern alone?
• 
  
• In ECG #3 — this unusually shaped coved segment (outlined in RED — highlighted by the BLUE arrow) is now even more prominent. I thought this coved segment to be more consistent with superimposed ST elevation from acute RV injury rather than solely the result of a Brugada-1 and/or Brugada-2 pattern.
• 
  
• BOTTOM LINE: As per Dr. Smith's discussion above — the markedly elevated serum troponin — as well as additional imaging studies confirmed RV Myocardial Contusion. While I believe the serial ECGs in today's case show variations of Brugada-1 and -2 Phenocopy — I suspect the BLUE arrows in Figure-1 highlight superimposed ST elevation from acute RV injury. That said, the "good news" — is that this patient should recover (and his ECG will most probably normalize as he does!).

 

Figure-1: Visual summary of ECG Patterns in Brugada Syndrome (adapted from the article by Brugada et al in JACC: Vol. 72; Issue 9; 2018) — A) Brugada-1 ECG pattern, showing coved ST-segment elevation ≥2 mm in ≥1 right precordial lead, followed by a negative T-wave. — B) Brugada-2 ECG pattern (the “Saddle-back” pattern) — showing concave-up ST-segment elevation ≥0.5 mm (generally ≥2 mm) in ≥1 right precordial lead, followed by a positive T-wave. — C) Additional criteria for diagnosis of a Brugada-2 ECG pattern (TOP: the ß-angle; BOTTOM: A Brugada-2 pattern is present if 5 mm down from the maximum r’ rise point — the base of the triangle formed is ≥4).

BELOW this summary of Brugada ECG Patterns — I've put together the V1,V2,V3 leads from the 3 serial ECGs obtained in today's case (See text).

A man in his 40s with multitrauma from motor vehicle collision

Submitted and written by Andrew Yde MD, peer reviewed by Meyers, Grauer, Smith



A man in his 40s presented after motor vehicle collision in which he was the unrestrained driver in a vehicle moving at high speed. He was found by EMS to be obtunded at the scene of the accident, and was intubated in the field. On initial ED evaluation the patient was found to be hypotensive and tachycardic, with multiple obvious orthopedic injuries. He received emergent transfusion and bilateral chest tubes. FAST exam was indeterminate, but did not show a large amount of free fluid. He was deemed stable for CT scans.

CTs revealed the following injuries: left hemopneumothorax, right pneumothorax, pneumomediastinum, sternal fracture, right anterior rib fractures 2-6, left sided flail chest of ribs 2-9, L2 transverse process fracture, left clavicle fracture, grade 1-2 liver laceration, and a grade 1 splenic laceration. The patient was admitted to the surgical trauma ICU.


That night, he exhibited multiple episodes of ectopy, and what appeared to be NSVT. Electrolytes were found to be within normal limits, and the following EKG was obtained:

What do you think?

 

The patient had no prior EKGs in the system for comparison. The ECG shows sinus rhythm with a right bundle branch block (RBBB). The STD and T waves following the RBBB in V1-V3 are unusual in morphology and potentially excessively discordant compared to normal RBBB. Also, the lateral precordial leads are unusual in that they still have the R', instead of the slurred S wave we see in I and aVL, suggesting that the lateral chest leads are misplaced medially (probably because of the left chest tube in place).

Cardiac contusion was suspected. Remember: other important considerations for ECG changes in the setting of trauma include traumatic coronary dissection or laceration.

A troponin was ordered, along with a repeat EKG, seen below.

Mostly unchanged.

 

The high sensitivity troponin I (normal less than 20 ng/L) resulted at 20,973 ng/L, and cardiology was consulted. Cardiology recommended an echocardiogram and trending troponins, stating that cardiac contusion was their initial impression. 

The repeat troponin overnight into the following morning was＞25,000 ng/L (the lab does not report higher values).

By this time, a formal echocardiogram had been obtained, which revealed normal left ventricular ejection fraction (LVEF), with a severely hypokinetic right ventricle. These findings were interpreted as consistent with cardiac contusion. Cardiology continued to follow, but no cardiac catheterization was deemed necessary. Cardiology cleared the patient for rib plating.

After induction of anesthesia in the operating room, awaiting rib plating, the patient had a run of what was assumed to have been Non-Sustained Ventricular Tachycardia (NSVT), though this telemetry strip was not available for review. He then went into a bradydysrhythmia, and the procedure was aborted. On returning to the ICU, the ECG below was taken, revealing atrial fibrillation with a PVC.

Atrial fibrillation, narrower RBBB than before, one PVC. There appears to be STE and possibly hyperacute appearing T waves in some leads such as I, II, aVF, V6, compared to prior ECGs.

The troponin had begun to downtrend significantly, down to 2,243 ng/L. by hospital day 3. 

A repeat echocardiogram revealed no left ventricular wall motion abnormalities and normal EF, but reduced RVEF and akinesis of the RV free wall and mid ventricle to apex., with biatrial enlargement. The patient was placed on an amiodarone drip, and ultimately converted back to sinus rhythm. He remained hemodynamically stable.

More ECGs were obtained at days 6 and 9 below:

 

These ECGs show progressive resolution of the RBBB and significant improvement in prior concerning ST changes. 

The remainder of the patient’s hospital course was characterized by many complications. He was finally discharged to rehab after about a month in the hospital.


See our other cases of myocardial contusion and related cases (some of which have an important diagnosis OTHER THAN myocardial contusion!):

A Child with Blunt Trauma -- See how the ECG can be definite for myocardial contusion, but subtle, and what happens if you miss it.   

Massive Transfusion for Motorcycle Collision with Hemorrhage, Troponin Elevated.

ECG of pneumopericardium and probable myocardial contusion shows typical pericarditis

Male in 30's, 2 days after Motor Vehicle Collsion, complains of Chest Pain and Dyspnea

Head On Motor Vehicle Collision. ST depression. Myocardial Contusion?

Gunshot wound to the chest with ST Elevation

Would your radiologist make this diagnosis, or should you record an ECG in trauma?

Blunt Trauma in a Child

40-something male in a head-on Motor Vehicle Collision and Splenic Injury

Discussion

This is a case where clinical context is of vital importance, because the EKG manifestations of cardiac contusion are fairly unpredictable. Intramyocardial hemorrhage, edema, and necrosis of myocardial muscle cells are characteristics of cardiac contusion. All of these cause troponin elevation, making troponin a very specific marker for cardiac injury. It is suggested that a troponin that is within normal reference range at about 4-6 hours from the inciting event suggests strongly the absence of cardiac injury in blunt chest trauma (Sybrandy).

The EKG is not generally sensitive for cardiac contusion. The right ventricle comprises the majority of the anterior heart which is most susceptible to direct injury in blunt chest trauma. Cardiac contusion can manifest on the ECG in a number of ways, including: ST segment elevation or depression, prolonged QT, new Q waves, conduction disorders such as RBBB, fascicular block, atrioventricular (AV) nodal conduction disorders (1,2, and 3 degree AV block), and arrhythmias such as sinus tachycardia, atrial and ventricular extrasystoles, atrial fibrillation, ventricular tachycardia, ventricular fibrillation, sinus bradycardia, and atrial tachycardia (Sybrandy). RBBB in blunt chest trauma seems to be indicative of several RV injury. Atrial fibrillation is also a predictor of worse outcomes in this case (Alborzi).

See these publications for more information

Overall, management for cardiac contusion is mostly supportive unless surgical complications develop, involving appropriate treatment of dysrhythmias and hemodynamic instability. Ultimately, a normal ECG and normal troponin at 4-6 hours from initial traumatic incident is highly predictive of a lack of future cardiac complications in blunt chest trauma. Between 81-95% of life-threatening ventricular dysrhythmias and acute cardiac failure occur within 24-48 hours of hospitalization. Troponins and EKGs should be trended until normalization (Sybrandy).  

Delayed cardiac rupture is a potential consequence, especially if there is any ST Elevation.  See this case, this case, and this case.  In patient's at risk, physical activity should be limited for several months after the injury.




References

Alborzi, Z., Zangouri, V., Paydar, S., Ghahramani, Z., Shafa, M., Ziaeian, B., Radpey, M. R., Amirian, A., & Khodaei, S. (2016, April 13). Diagnosing myocardial contusion after blunt chest trauma. The journal of Tehran Heart Center. Retrieved July 2, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5027160/

Moyé, D. M., Danielle M. Moyé From the Division of Cardiology, Dyer, A. K., Adrian K. Dyer From the Division of Cardiology, Thankavel, P. P., Poonam P. Thankavel From the Division of Cardiology, & The Data Supplement is available at http://circimaging.ahajournals.org/lookup/suppl/doi:10.1161/CIRCIMAGING.114.002857/-/DC1.Correspondence to Poonam Punjwani Thankavel. (2015, March 1). Myocardial contusion in an 8-year-old boy. Circulation: Cardiovascular Imaging. Retrieved July 2, 2022, from https://www.ahajournals.org/doi/10.1161/CIRCIMAGING.114.002857

Sybrandy, K. C., Cramer, M. J. M., & Burgersdijk, C. (2003, May). Diagnosing cardiac contusion: Old Wisdom and new insights. Heart (British Cardiac Society). Retrieved July 2, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1767619/ 

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MY Comment by KEN GRAUER, MD (8/6/2022):

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

Excellent review by Drs. Yde and Meyers — regarding multi-trauma with resultant Cardiac Contusion! I focus my comment on a number of additional specific aspects of the serial ECGs obtained in today's case.

As per Drs. Yde and Meyers — the ECG is less than optimally sensitive for detecting cardiac injury following blunt trauma. This is because the anterior anatomic position of the RV (Right Ventricle), and its immediate proximity to the sternum — makes the RV much more susceptible to blunt trauma injury than the LV. But because of the much greater electrical mass of the LV — electrical activity (and therefore ECG abnormalities) from the much smaller and thinner RV are more difficult to detect. To REVIEW (Sybrandy et al: Heart 89:485-489, 2003 — Alborzi et al: J The Univ Heart Ctr 11:49-54, 2016 — and Valle-Alonso et al: Rev Med Hosp Gen Méx 81:41-46, 2018) — ECG findings commonly reported in association with Cardiac Contusion include the following:

• None (ie, The ECG may be normal — such that not seeing any ECG abnormalities does not rule out the possibility of cardiac contusion).
• Sinus Tachycardia (common in any trauma patient ...).
• Other Arrhythmias (PACs, PVCs, AFib, Bradycardia and AV conduction disorders — potentially lethal VT/VFib).
• RBBB (as by far the most common conduction defect — owing to the more vulnerable anatomic location of the RV). Fascicular blocks and LBBB are less commonly seen.
• Signs of Myocardial Injury (ie, Q waves, ST elevation and/or depression — with these findings suggesting LV involvement).
• QTc prolongation.
• 
  
• NOTE: Prediction of cardiac contusion "severity" on the basis of cardiac arrhythmias and ECG findings — is an imperfect science.

Additional KEY Points:

Despite the predominance for RV (rather than LV) injury — use of a right-sided V4R lead has not been shown to be helpful compared to use of a standard 12-lead ECG for detecting ECG abnormalities.

• In addition to ECG abnormalities related to the blunt trauma of cardiac contusion itself — Keep in mind the possibility of other forms of cardiac injury in these patients (ie, valvular injury, aortic dissection, septal rupture) — as well as the possibility of a primary cardiac event (ie, acute MI may have been the cause of an accident that led up to the trauma).
• ECG abnormalities may be delayed — so repeating the ECG if the 1st tracing is normal is appropriate when concerned about severe traumatic injury.
• That said (as per Drs. Yde and Meyers) — IF troponin is normal at 4-6 hours and IF the ECG is normal — then the risk of cardiac complications is extremely low.

How Did YOU Interpret the Initial ECG?

I found the initial ECG in today's case extremely interesting. Clearly, this patient with severe multi-trauma following a motor vehicle accident suffered a cardiac contusion — confirmed by the presence of obvious ECG abnormalities and marked troponin elevation.

• While the literature acknowledges the difficulty trying to predict "severity" of cardiac contusion from ECG findings — there are a number of concerning ECG abnormalities present in the initial tracing (Figure-1).

Figure-1: I've reproduced and labeled the initial ECG in today's case.

MY Thoughts on the Initial ECG:

• The rhythm in ECG #1 is sinus (RED arrow in lead II) — at a rate of ~90/minute. 
• The PR interval looks to be slightly prolonged (especially considering the relatively rapid rate). Among the conduction defects seen with cardiac contusion is 1st-degree AV block.
• The QRS complex is widened — and the predominantly wide qR pattern in lead V1, in association with the wide terminal S wave in lead I — is diagnostic of RBBB (Right Bundle Branch Block).
• 
  
• NOTE: The ECG in Figure-1 provides an excellent example of how QRS width may vary depending on which lead is being looked at. I've added vertical time lines to clarify the beginning and end of the QRS complex (RED and PURPLE dotted lines, respectively). Despite obvious QRS widening — Note how narrow the QRS looks in simultaneously-recorded lead II, due to the fact that much of the last part of the QRS in this lead lies on the baseline.
• 
  
• The QRS appears to be very wide and fragmented in leads V1,V2,V3. While I did not find literature to support this degree of widening and amorphous QRS morphology as a predictive factor of cardiac contusion severity — I thought the observation over serial tracings of progressive QRS narrowing, with return to a more normal triphasic RBBB morphology supported the concern regarding this initial tracing.
• Additional evidence of abnormal ECG findings in Figure-1 was present in the form of: i) Deep Q waves in leads III and aVF; ii) Overly peaked (hyperacute?) T waves in leads I, II, aVL and aVF; and, iii) Excessive ST-T wave depression in the anterior leads (that clearly exceeds that expected with simple RBBB).
• 
  
• Did YOU notice how atypical the lateral chest leads are for RBBB? (QRS complexes within the dotted BLUE rectangles). Normally with RBBB — lateral chest leads show an upright R wave with a wide terminal S wave — and not persistence of similar-looking triphasic-notched complexes with persistent ST-T wave depression. I suspect the reason for this atypical QRST morphology in leads V4,V5,V6 — is that electrode lead placement had to be altered in this patient with multi-thoracic traumatic injuries requiring chest tubes, splinting, bandages, etc. NOTE: The relevance of recognizing this atypical RBBB morphology relates to its potential effect on comparing serial ECGs.
• 
  
• Did YOU notice the prominent J waves (? Osborn waves) in the inferior leads? There is also prominent negative notching in leads I and aVL (BLUE arrows in the limb leads). We've previously noted how such prominent J waves may be seen not only with hypothermia — but also with other conditions, including myocardial ischemia — and that ischemia-induced J-waves have been found to increase the risk of developing malignant ventricular arrhythmias (See My Comment in the September 23, 2020 post of Dr. Smith's ECG Blog). 
• J waves have also been shown to be a marker of significant increased risk following penetrating cardiac trauma (Nicol and Navsaria: J Injury 45:112-115, 2014). 
• Regardless of whether you call these deflections prominent J waves or Osborn waves — I found it "telling" that these deflections were present in both of the first 2 ECGs done in today's case — that an episode of presumed VT, followed by significant bradycardia was seen shortly thereafter in the OR — but that these J-point deflections were no longer seen in the last 3 ECGs (which were done after those life-threatening arrhythmias resolved).

What Happened on Serial ECGs?

I've selected 3 of the 5 ECGs from today's case with the goal of highlighting the evolution of ECGs changes that developed over the course of this patient's hospital admission (Figure-2).

Figure-2: Comparison between 3 of the 5 ECGs recorded in today's case.

MY Thoughts on these Serial ECGs:

I found it interesting to trace progressive improvement of ECG abnormalities over the course of this patient's hospital admission:

• I've already discussed the notable findings in ECG #1.
• 
  
• ECG #3 — was obtained following the episode of presumed VT and marked bradycardia that necessitated stopping the operative procedure. Compared to ECG #1, there is now: i) AFib with a PVC; ii) Some narrowing of the QRS, with appearance of a more distinct triphasic complex in anterior leads (that is now much more typical of RBBB morphology); iii) Much less ST-T wave depression in the anterior leads; iv) Development of significant ST elevation in leads I and II (and to a lesser extent in leads aVL and aVF); v) Loss of the prominent J-point notching that was seen in ECG #1; and, vi) A change in QRS morphology in the lateral chest leads that seems more consistent with an RBBB conduction defect (perhaps a result of improved electrode lead placement?).
• 
  
• ECG #4 (done on Hospital Day #6) — There is now: i) Return to normal sinus rhythm at a slower rate; ii) Further narrowing of the QRS — that is now consistent with an incomplete RBBB pattern; iii) Reduced size of the Q wave in lead III — with resolution of the Q wave in lead aVF; and iv) Continued improvement in ST-T wave abnormalities.
• 
  
• In SUMMARY: While the literature does not provide us with specific ECG criteria for assessing severity of cardiac contusion — today's case does provide insight as to how clinical correlation with serial ECGs can confirm that the patient is recovering. I thought it significant that this severely injured multi-trauma patient initially showed an extremely wide QRS (with RBBB and an amorphous QRS morphology) — that gradually narrowed and took on a more distinct RBBB morphology (with eventual resolution of the conduction defect). Along the way — the patient manifested ST-T wave elevation and depression, changing size of Q waves, and a series of rhythm changes (VT, bradycardia, AFib, PVCs) — with eventual improvement of all these ECG findings that corresponded with his progressive recovery.

ST elevation after gunshot to the chest

Submitted and written by Bobby Nicholson MD, peer reviewed by Meyers, Grauer, McLaren, and Smith

A young man suffered multiple gunshot wounds. He complained of worsening dyspnea en route to the emergency department and was placed on nonrebreather facemask. On initial exam he had penetrating wounds to the left chest with a rigid abdomen and superficial wounds to the lower extremities. E-FAST examination showed bilateral lung sliding with a small pericardial effusion without evidence of tamponade. He was taken emergently to the operating room where he underwent exploratory laparotomy with subxiphoid pericardial window, median sternotomy, and repair of penetrating cardiac injury to the apex of the left ventricle along with repair of multiple intraabdominal injuries.

Here is part of his operative report:

"There was a left central diaphragmatic injury with ongoing bleeding consistent with decompressing hemopericardium. Subxiphoid pericardial window was performed confirming hemopericardium. Thus median sternotomy was performed. Hemopericardium was evacuated. Heart was examined with note of a penetrating injury to the apex of the left ventricle. There was moderate surrounding contusion and active bleeding. Given injury pattern and location, primary repair with sutures was performed. A total of 2 horizontal mattress pledgeted sutures were placed. There was no apparent involvement of the cardiac vessels."


On hospital day 1, the following EKG was obtained:

What do you think? What diagnoses should be on the differential given the known injury pattern?



There is frank ST elevation in multiple leads (V4-6, I, II, III, aVF) with reciprocal STD in aVR and V1. Some leads have accompanying large T waves suspicious for hyperacute T waves, while others like lead aVF have a distinct appearance of STE without large T waves (in pericarditis we sometimes discuss the ST / T ratio, as classic OMI typically has large T waves and large STE, while pericarditis sometimes has relatively small T waves compared to the STE).

Given the known gunshot wound to the heart, the differential could include: direct injury/occlusion of an epicardial coronary artery (such as the LAD) causing MI (including traumatic dissection), direct tissue trauma causing injury current manifesting as STE, or some kind of myopericarditis as a result of the injury, or multiple of these etiologies in combination.

The apex of the LV is most often supplied by the LAD, and OMI including the apex can sometimes cause confusion about the associated ECG leads. The most common and important pitfall is: large LAD occlusion often includes apical AMI, which can manifest OMI ECG findings in the "inferior" and/or "lateral" leads due to the relatively inferior and lateral position of the apex. The pitfall is that some providers will mistakenly believe that this pattern indicates "diffuse" STE, which makes them think more of pericarditis because classic ECG teaching advises that diffuse STE is indicative of pericarditis.

The down-sloping TP segment is referred to as Spodick's sign, and is most obvious in lead II.

In this study of Spodick sign and other potential discriminators between OMI and pericarditis, Spodick sign was noted (by a single expert, Dr. Mattu) in 5% of "STEMI" patients and 29% of "pericarditis" patients. 

A transthoracic echocardiogram was obtained which showed an LVEF of 55-60% with a trivial pericardial effusion. There was no evidence of tamponade or appreciable wall motion abnormality. The patient was treated with Toradol for his chest pain (presumably giving NSAIDs for anti-inflammatory action against pericarditis) and endorsed significant pain reduction.

No cath or CT angiogram was ever done.

No troponin was ever ordered. 

He underwent treatment of multiple traumatic injuries.

The following EKG was obtained after 5 days and showed normalization of the patient’s ST abnormalities.

The two ECGs above were the only ones ever performed during his hospitalization.

In addition to his traumatic injuries, this patient was ultimately diagnosed with traumatic uncomplicated pericarditis. He was eventually discharged from the hospital in stable condition. There has not been any available follow up information for this patient.

Learning Points:

This patient probably did not have acute coronary occlusion, but the workup performed would have been insufficient to detect acute coronary occlusion if he had suffered it. But they had direct visualization of the injured myocardium, which may also have high accuracy for ruling out coronary occlusion!

Traumatic injuries can cause direct damage to coronary arteries resulting thrombotic occlusion or dissection, which then causes OMI just like any other cause of acute coronary occlusion.

The only way to definitively rule out coronary occlusion in cases like this is angiography (perhaps in the future CT coronary angiogram could be perfect for this situation). MRI is good if you are not in a hurry, such as this case.

ECG changes of the apical myocardium may appear in the lateral leads V5-6 and inferior leads II, III, aVF.

Anytime there is a finding in multiple left sided leads, the opposite finding must be present in lead aVR.

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Comment by KEN GRAUER, MD (6/8/2022):

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The young man in today's case was lucky to have survived multiple gunshot wounds — including a penetrating wound to the heart. In addition to his traumatic injuries — he was discharged from the hospital with a diagnosis of traumatic uncomplicated pericarditis. Realizing that the circumstances of today's case are very different from the usual setting that prompts consideration of a diagnosis of acute pericarditis — I still thought the topic of the ECG Diagnosis of Acute Pericarditis to be a worthy one for our periodic review.

• I found it difficult to locate literature on specific ECG findings with traumatic pericarditis from penetrating cardiac trauma. As alluded to in the above discussion by Drs. Nicholson and Meyers — you might find almost anything on ECG, depending on the specific nature of cardiac injury (ie, there may be direct damage to coronary arteries resulting in acute thrombotic occlusion or dissection — pericardial effusion, possibly with tamponade — pneumopericardium — neighboring pneumothorax, including tension pneumothorax altering the relationship of anatomic structures — and/or cardiac contusion of varying severity).
• In contrast — a specific set of ECG findings has been described for non-traumatic acute pericarditis (See below). By way of perspective — despite being one of the most common considerations in international ECG forums — acute pericarditis is extremely uncommon in clinical practice.
• As has been emphasized many times on Dr. Smith’s ECG Blog — acute pericarditis is far less common than acute MI or a repolarization variant among patients who present to an emergency setting. As per Dr. Smith, “You diagnose acute pericarditis at your peril!" That said — it is good to keep in mind what the ECG criteria for this diagnosis are.

The Initial ECG in Today's Case:

For clarity — I've reproduced in Figure-1 the initial ECG in today's case. From a purely educational perspective — I thought it interesting to assess this initial ECG for findings consistent with a diagnosis of acute pericarditis — as well as for findings against that diagnosis.

Figure-1: The initial ECG in today's case.

ANSWERS:

• ECG findings in Figure-1 consistent with acute pericarditis include: i) Upward sloping ST elevation in multiple leads; ii) Spodick's sign (most obvious in lead II — as per Drs. Nicholson and Meyers); and, iii) The ST-T wave ratio in lead V6 is >0.25 (whereas it tends to be less than this with repolarization variants).
• 
  
• Of no diagnostic help in Figure-1 is the finding of PR depression — which is seen in some but not other leads (ie, it is present in leads II, V4,5,6). Even if PR depression was more diffuse — the specificity of this finding for acute pericarditis is modest at best.
• 
  
• ECG findings in Figure-1 against the diagnosis of acute pericarditis include: i) There is a fairly large Q wave with ST elevation and T wave inversion in lead III that resembles the picture of acute MI (whereas with acute pericarditis — Q waves should not be seen — and T wave inversion typically does not begin until ST elevation has resolved); and, ii) ST elevation is lacking in leads aVL, V2 and V3 (The ST segment straightening in leads aVL and V3 is much more characteristic of coronary disease than acute pericarditis).

Conclusion: The ECG in Figure-1 would not be typical for non-traumatic acute pericarditis. However, it could be consistent with traumatic pericarditis (because ECG findings are so variable in traumatic pericarditis).

• NOTE: The ECG features of acute myocarditis may differ substantially from those of a "pure" pericarditis. There may be a resemblance between these 2 entities — but ST segment deviations (elevation and depression) with myocarditis may not follow the timing seen with pericarditis. In addition, Q waves may develop — so at times it may be difficult to distinguish myocarditis from infarction on ECG.

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ECG Findings of Acute Pericarditis:

By way of Review — I’ve excerpted in Figure-2, relevant paragraphs from a 2017 ESC (European Society of Cardiology) article on this subject by Xanthopoulos & Skoularigis (ESC: Vol. 15, No.15-9/6/2017).

• CLICK HERE — for a 9-page PDF of "My Take" on the ECG diagnosis of acute pericarditis.

Figure-2: Excerpt from ESC review on acute pericarditis (See text).

Among the KEY points regarding ECG diagnosis of acute pericarditis from Figure-2 (to which I’ve added some of my own points) — are the following:

• Typical ECG findings of acute pericarditis are not always present! The ECG is far from a perfect diagnostic tool.
• 4 Stages are described in the ECG evolution of Acute Pericarditis findings. These can be summarized as: i) Stage I — in which there is generalized ST elevation in most leads (except perhaps in the “right-sided” leads = leads III, aVR and V1); ii) Stage II — in which this generalized ST elevation returns to baseline (ie, “pseudo-normalization” phase); iii) Stage III — in which there is diffuse T wave inversion; and, iv) Stage IV — in which the overall tracing normalizes.
• Of these 4 stages — only Stage I is readily recognizable as potentially due to acute pericarditis. You would never guess “pericarditis” if given an isolated tracing from Stage II, III or IV.
• The time course of these 4 ECG Stages (in those pericarditis cases in which they occur) — is highly variable. The ESC summary in Figure-2 states that Stage I may last “between hours to days” — before evolving into Stage II.
• The shape of the ST elevation is typically concave-up (ie, a “smiley” configuration).
• ECG signs usually associated with acute MI (ie, abnormally large or wide Q waves — reciprocal ST depression) are absent!
• 
  
• PEARL: The appearance of the ST-T wave in lead II tends to resemble that in lead I with acute pericarditis. In contrast, with acute MI — ST-T wave appearance in lead II resembles lead III (and not lead I).
• There may be PR depression in many leads — with “reciprocal” PR elevation in lead aVR.
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• The RATIO of the amount of ST elevation to T wave amplitude in lead V6 should be more than 0.25 (ie, height of the ST elevation, as measured from the end of the PR segment to the J-point — should be more than 1/4 of the height of the T wave in lead V6 — as shown below in Figure-3).

Figure-3: Illustration of how the ST segment to T wave ratio is calculated — adapted from Life-In-The-Fast-Lane (and taken from My Comment in the December 13, 2019 post of Dr. Smith's ECG Blog).