Saturday, August 6, 2022

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.   















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/ 






===================================
MY Comment by KEN GRAUER, MD (8/6/2022):
===================================
Excellent review by Drs. Yde and Meyers — regarding multi-trauma with resultant Cardiac ContusionI 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; andiii) 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; andvi) 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.




Wednesday, August 3, 2022

What happens if you don't recognize Hyperacute T-waves?

The origin of these ECGs cannot be revealed.  


Time 0:

Sinus rhythm with an intraventricular conduction delay (QRS is about 120 ms)

Hyperacute T-waves in V2-V5, Diagnostic of Proximal LAD occlusion, but without ANY ST Elevation except for less than 1 mm in aVL, and 0.25 mm in lead I.

There is also minimal STE in aVL with reciprocal STD in II, III, aVF.

Notice that there is plenty of R-wave in V2 and V3.

This should be an obvious case of acute proximal LAD Occlusion.  However, it was missed.

In this, case the Hyperacute T-waves are preceded by subtle ST Depression in V2 and V3.  Thus, they are specifically the hyperacute T-waves called "de Winter's T-waves."

Note that hyperacute T-waves are not just tall.  In fact, they frequently are NOT tall.  They are "bulky" and this bulk is always in proportion to the QRS.

"Bulk" is a result of the area under the curve (AUC), in proportion to the QRS amplitude/AUC.

Such high AUC is a result of:
1) JT interval (total duration of T-wave)
2) Degree of upward concavity
3) Symmetry
4) Amplitude


Old ECG:

Ventricular Paced Rhythm with some native beats which show inferior OMI.  
(There is a also a pacer spike in the midst of the native QRS -- it comes to late to pace the ventricle)
The paced beats in V2 and V3 show posterior OMI


3 hours:

T-waves remain hyperacute, but not as tall.  
Q-waves developing in V2-V4 and aVL.  
QS-wave in V2.


12 hours:

T-waves slightly less prominent
Q-waves definite


21 hours

T-waves much less prominent, which is evidence that there is less viable ischemic myocardium.
It is possible that there is some reperfusion as etiology of resolving ST Elevation.  Evidence for this is the abrupt downturn of the T-wave. 
But any reperfusion is AFTER significant myocardial loss, as evidenced by QS-wave in V2 and new QR-wave in V3

I do not have the corresponding angiogram, troponins, echo.  But these ECGs definitively show the irreversible loss of myocardium that happens if Hyperacute T-waves go unrecognized.  They are a definite sign of OMI, and if the patient does not have reperfusion (either by lucky spontaneous reperfusion or by intervention), then lots of myocardium will be lost.

Result: lots of lost myocardium.


See here for many examples of hyperacute T-waves:











===================================
Comment by KEN GRAUER, MD (8/3/2022):
===================================
An important part of the process of assessing serial ECGs — is comparison with a prior ("baseline" ) tracing. The goal of determining which changes are new was instantly evident in today's case by review of the old ECG ( = the 2nd ECG shown above in Dr. Smith's discussion of this patient's serial tracings).

I found the Old ECG in today's case to be fascinating — so I focus my comment on its analysis. For clarity — I've reproduced this 2nd tracing in Figure-1. At the time this Old ECG was done — the patient had a pacemaker. As per Dr. Smith — the rhythm in ECG #2 shows intermittent ventricular pacing with evidence of infero-postero infarction at some point in time.

QUESTIONS:
No clinical information was available in association with the ECG in Figure-1. All we know — is that this ECG was recorded at some point in the past.
  • How would you date the infarction in Figure-1?
  • Is the pacemaker functioning appropriately?
  • What is the underlying cardiac rhythm? (ie, WHY do you think the pacemaker was needed?).

Figure-1: The previous ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).


MY Thoughts on the Old ECG:
The art and science of cardiac pacing continues with breathtaking advances. It is no longer easy (or even possible) to fully assess pacemaker function solely from the ECG without knowledge of pacing specifications for that particular patient. That said — we often can get a quick idea as to how a pacemaker is functioning, especially when one or more spontaneous beats are present. For the ECG that appears in Figure-1 — there is more to be learned!
  • The "good news" — is that modern pacemakers can be interrogated remotely by means of a wireless, telemetered, external programming device (Brief review by Safavi-Naeini and Saeed — Texas Heart Inst J 43:415-418, 2016 on the basics of pacemaker troubleshooting).
  • The 2nd piece of "good news" — is that modern pacemakers are truly amazing devices with an astonishing performance record. Pacemaker malfunction does occur (and it is important to recognize this when it happens) — but most of the time, the pacemaker will be right! So I generally begin my assessment of pacemaker tracings with the mindset that even when I see unusual or unexpected findings — there may be a physiologic reason for why the pacemaker is appropriately functioning in this way (the details of which can then be sorted out when the pacemaker is interrogated).

Assessing the Pacemaker:

In Figure-2 — I've labeled the long lead II rhythm strip from ECG #2.

  • RED arrows in Figure-2 reveal that there is an underlying regular sinus rhythm in ECG #2. Note that the PR interval that precedes each of the narrow beats (ie, beats #1, 4, 7) is the same! Therefore — beats #14 and 7 are sinus-conducted (albeit with a prolonged PR interval of 0.24 second = 1st-degree AV block).
  • The vertical PINK lines in Figure-2 highlight pacemaker spikes. The fact that wide, paced complexes immediately follow pacemaker spikes to produce beats #2,3; 5,6; and 8 — confirms that there is at least some ventricular capture!
  • The R-R interval of the first 3 pacemaker spikes is 6 large boxes. This corresponds to a pacing rate of 50/minute — which presumably is the rate the pacer was set at to fire if no spontaneous beats are sensed.

WHY does the 4th pacer spike occur early?
  • Note that beat #4 is a spontaneous sinus-conducted beat! If the pacemaker was only sensing the QRS — then we would not see this 4th pacemaker spike that occurs just after beat #4!
  • As stated a moment ago — spontaneous beats in Figure-2 are conducting with a prolonged PR interval. So it must be that the reason the 4th pacer spike in Figure-2 occurs early — is that there is dual chamber pacing (of both atria and ventricles) — and since no QRS complex was sensed after 0.23 second at this point in the cardiac cycle, the pacemaker fired. The 7th pacer spike in Figure-2 also occurs early for the same reason. This implies that the pacemaker is appropriately sensing the atria. (Simple adjustment could reprogram the pacer to accept a slightly longer PR interval before firing).
  • That the pacer is appropriately sensing the ventricles — is evident from the 5th pacer spike — which once again waits the programmed amount of 6 large boxes after the previous pacer spike before firing. This provides the patient with a guaranteed ventricular rate of at least 50/minute — while still providing adequate opportunity for spontaneous conduction to occur.


Figure-2: I've labeled P waves (RED arrows) and the pacemaker spikes (PINK lines) that are seen in the long lead II rhythm strip from ECG #2.


How to "Date" the Infarction in Figure-1?
Now that we've determined from Figure-2 that beats #1, 4 and 7 are spontaneously conducted — We can return to Figure-1 to assess QRS morphology of these sinus-conducted beats.

  • Focusing on beat #1 in leads II and III — reveals a large Q wave in lead III. The ST-T wave of these beats (as well as the ST-T for sinus-conducted beat #4 in lead aVF) looks hyperacute, albeit without frank ST elevation.
  • Sinus-conducted beat #4 in lead aVL manifests reciprocal change (ie, mirror-image opposite ST-T wave depression — compared to the ST-T wave appearance in lead III). This suggests a recent inferior OMI (perhaps just after the stage of ST elevation). The hint of terminal T wave positivity in aVL (and of beginning T wave inversion in the inferior leads) may portend reperfusion.
  • No spontaneous beats are seen corresponding to the 2 QRS complexes in leads V1,V2,V3 — but ST-T wave morphology of paced beats #5 and 6 suggests abnormal ST segment flattening with excessive T wave peaking (that is also seen for beat #8 in lead V4). I interpreted this ST-T wave appearance as indicative of posterior OMI reperfusion T waves.

  • BOTTOM Line: My hunch is that there was a recent infero-postero OMI — and that we are now see reperfusion changes.


What is the Underlying Rhythm in Figure-1?
So WHY was the pacemaker needed for ECG-2? The answer to this is best explained by laddergram (Figure-3):

  • For clarity — I labeled the sinus-conducted P waves in Figure-3 with RED arrows.
  • YELLOW arrows highlight those P waves that are not conducted. Since some P waves are conducted but others aren't — some form of 2nd-degree AV block is present.

  • PEARL: Since we know this patient has just had an infero-postero OMI — and there is group beating with sinus-conducted beats that manifest a narrow QRS with 1st-degree AV block — the odds are overwhelming that the type of conduction disturbance will turn out to be 2nd-degree AV block of the Mobitz I Type ( = AV Wenckebach)!

  • GREEN arrows highlight non-conducted P waves that do not have a "chance" to conduct — because they either occur just before or just after paced beats.
  • The small BLUE circles at the bottom of the laddergram correspond to pacer spikes. As already noted — the pacer spikes that appear just after sinus-conducted beats #1, 4 and 7 are appropriately sensing the preceding P wave — but do not pace the ventricles because of sinus conduction.

  • BOTTOM Line: It is impossible to tell IF the GREEN arrow P waves would be able to conduct if given a chance to do so (which is why I added ??? in the AV nodal Tier of the laddergram). That said — as per the above Pearl — statistical odds overwhelmingly favor Mobitz I 2nd-degree AV block as the conduction disturbance — with the "good news" that AV Wenckebach in this setting often resolves as the patient's condition stabilizes.


Figure-3: My proposed laddergram for the rhythm in ECG #2 from Figure-1.





Monday, August 1, 2022

A man in his 60s with dizziness, nausea, chest pain, and LBBB

Submitted and written by Parker Hambright MD, peer reviewed by Meyers, McLaren, Grauer, Smith


A man in his late 60s called EMS for acute dizziness, nausea, vomiting, and chest pain shortly after beginning his morning exercise. The symptoms lasted for only about 15 minutes and then resolved spontaneously. He was brought to the ED and evaluated in less than one hour from onset of symptoms. His history included known CAD, HTN, HLD, prior MI with LAD stent, AAA repair, and reported dizziness/vertigo.

Here are his EMS and ED triage ECGs (unclear whether symptoms still present or resolved at time of these ECGs, but it seems that symptoms were likely improved or resolved):

EMS:


ED triage (within 1 hour of onset of symptoms):




Baseline ECG from 1 year ago:
This baseline ECG shows a normal LBBB.



Meyers interpretation: The EMS and triage ECGs above have suspicious, but not diagnostic, changes from the baseline ECG. The baseline ECG shows only minimal ST deviations in the limb leads, whereas the triage ECG shows greater ratios of STE in III and aVF and STD in I and aVL, with increased area under the T waves, compared to baseline. But the triage ECG does not have any of the modified Sgarbossa criteria. It is not diagnostic, but potentially suspicious for dynamic changes of the inferior leads signaling inferior OMI. I would not yet be certain from these ECGs alone, but I would certainly get more information including repeat ECGs to see if this concern is playing out.


His initial high sensitivity troponin I (Beckman Coulter Access hsTnI) was less than 6 ng/L (drawn at about 1 hour from onset of symptoms).

The providers seemed to think that his symptoms were more related to his history of vertigo. He was given meclizine and symptoms had improved. He was discharged home.



.............


5 days later he returned complaining of two or three days of intermittent chest pain. He presented when he realized the pain wasn't going away during this most recent episode. He did not have further episodes of dizziness.

Here is his ECG at triage on second presentation:




The ECG above is diagnostic of inferoposterior OMI in LBBB. Findings include concordant STE in II, proportionally excessively discordant STE in III (ST/S ratio = 2/4 = 0.5) and aVF  with reciprocal depression in I and aVL, hyperacute T wave morphology in II, III, and aVF, and concordant STD with TWI in V1 and V2. The cath lab was activated and the patient was emergently taken by cardiology to the cath lab.


Angiography demonstrated a 70% stenosis of the proximal RCA and thrombotic (100%) occlusion of the mid RCA. Both lesions were stented and demonstrated TIMI 3 flow after intervention. The prior LAD stent was widely patent, and the LCX had only minor irregularities.



Grossly patent left main, LAD, and LCX.


Acute Mid RCA occlusion.


After initial intervention.

Post intervention.



Troponin I was 3,710 ng/L, then 8,228 ng/L, then no further troponins were 
measured.




Post cath ECG1:
Less STE and terminal T-wave inversion in inferior leads 
("Inferior" Pattern A Wellens' waves in the presence of LBBB)

Post cath ECG2:
T-waves have evolved to deeper and more symmetric.
("Inferior" Pattern B Wellens' waves in the presence of LBBB)


The post cath ECGs show inferoposterior reperfusion.


Echocardiogram demonstrated an LVEF of 50% with hypokinesis of the basal inferoseptal segments.


The patient experienced resolution of symptoms, was placed on DAPT, and was discharged on hospital day 2 following an uncomplicated hospital course.




Learning Points:

Use the modified Sgarbossa criteria to help diagnose OMI in the setting of wide QRS complexes such as LBBB and ventricular paced rhythm. But just like all other OMI ECG findings, the ECG starts from normal/baseline and evolves into these diagnostic findings in real time. The first visit ECG in this case is "between" the baseline and the diagnostic inferoposterior OMI ECG; in other words, since we know the pain was resolving, it is likely "on the way down" from more diagnostic OMI findings, on the way back to normal (and then likely reperfusion). Becoming accurate at ECG interpretation for OMI involves learning these progressions. Additionally, we have discussed many times on the blog that the ratio of 25% for excessive discordant STE is more specific but less sensitive than 20%. No criteria are perfect in isolation, and if you understand the OMI progression you will be able to perform better than the modified Sgarbossa criteria alone.

Not even high sensitivity troponins reliably show elevations within the first 1 or possibly even 2 hours since onset of ACS. It is very likely that a second troponin on this patients initial visit would have had a significant "delta" (change, or rise), or even risen above the 99th percentile upper reference limit.  In either case, further investigation would have been required.





Review of LBBB OMI Findings on ECG:

The approach to diagnosing OMI in the presence of LBBB was formerly through the use of the Original Sgarbossa criteria, published in 1996. They consist of the following 3 criteria:

Concordant ST elevation >1mm in at least one lead with positive QRS (5 points)
Concordant ST depression >1mm in at least one of leads V1-V3 (3 points)
Discordant ST elevation >5mm in at least one lead with negative QRS (2 points)

A total of 3+ points was deemed diagnostic of any acute MI (OMI or NOMI) OMI with a sensitivity of 49% and specificity of 99%. A subsequent meta-analysis published a sensitivity of only 20%. So although the original Sgarbossa criteria carried high specificity, it lacked sensitivity. This low sensitivity was because 1) the studies used biomarker diagnosis of MI (any MI), and did not use angiography (diagnosis of OMI) and 2) they did not use the principle of proportionality.

In 2012, Dr. Smith published a new criterion of “discordant STE >1mm AND >25% S wave amplitude” to substitute the previous criterion of “discordant STE >5mm in leads with negative QRS”.  The outcome was "Occlusion," and not just any acute MI. The new modified Sgarbossa criteria consists of the following 3 criteria:

Concordant ST elevation >1mm in at least one lead with positive QRS
Concordant ST depression >1mm in at least one of leads V1-V3
Discordant ST elevation >1mm AND >25% of the preceding S-wave amplitude in at least one lead

This alteration of the criteria removed the arbitrary 5mm STE cutoff and replaced it with a criterion that uses disproportional discordance, rather than a fixed amount of STE. The modified Sgarbossa criteria has been retrospectively validated 
by Meyers et al. and determined, using the 25% rule, to have a sensitivity of 80% and specificity of 99% for OMI; when the 20% rule is used, sensitivity rises to 84%, with specificity dropping to 94%.  This alteration improved sensitivity for OMI in LBBB - particularly in ECGs with low voltage - while not resulting in a statistically significant loss of specificity.


The modified Sgarbossa criteria can be objectively applied to ECGs with LBBB in the setting of ACS symptoms in attempts to identify OMI vs NOMI. A conceptual understanding of the criteria, however, can aid in determining which coronary vascular distribution is most likely to be experiencing an OMI. At the foundation of the OMI progression sequence, some degree ST elevation is expected to occur with an occlusive thrombus involving the anterior, lateral, and inferior walls of the myocardium and ST depression of V1-V4 is expected in posterior wall occlusions. These ischemic changes can also be anticipated in a pre-existing LBBB. The expected ECG changes for OMI in LBBB or ventricular-paced rhythm for the various coronary distributions are listed:


--Anterior (assuming predominantly negative QRS complex): Discordant ST elevation >1mm AND >25% S-wave amplitude in V1-V4
--Lateral (assuming predominantly positive QRS complex): Concordant ST elevation >1mm in leads V5-V6, I, or aVL
--Inferior: Concordant ST elevation >1mm or excessively discordant STE greater or equal to 25% in leads II, III, or aVF, based on QRS 
--Posterior (assuming predominantly negative QRS complex in anterior leads): Concordant ST depression >1mm in V1-V3


In an uncomplicated LBBB, abnormal depolarization of the ventricles results in abnormal repolarization and a ST segment discordance of approximately 10% is expected and normal. The recognition of concordant ST segment changes or disproportionally discordant ST segment changes (>25%) as abnormal and concerning for ischemia is paramount to the diagnosis of OMI in LBBB.

In this case, the ECG demonstrated 2 out of 3 of the modified Sgarbossa criteria. The prompt recognition and application of the modified Sgarbossa criteria allowed for timely revascularization and a promising clinical outcome.



See these other LBBB posts:

LBBB: Using the (Smith) Modified Sgarbossa Criteria would have saved this man's life





Acute Chest pain with LBBB. What is going on?










Some Cardiologists still are not familiar with Sgarbossa Criteria.....















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MY Comment, by KEN GRAUER, MD (8/1/2022):

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I am always intrigued by the challenge of interpreting the ECG of a patient with new symptoms and LBBB. Sometimes this assessment is EASY — as was the case for the 4th tracing in today’s case, obtained at the time this patient returned to the ED 5 days later — at which time, the ECG had become clearly diagnostic of acute infero-postero OMI. 
  • In contrast — ECG findings were far more subtle for the 2nd tracing in today's case (which was the initial ED Triage ECG).

As I have often noted in Dr. Smith’s ECG Blog — I favor a "QualitativeApproach for assessment of LBBB tracings in patients with new symptoms, especially when modified Smith-Sgarbossa Criteria are not yet satisfied.

  • I focus My Comment in today's case on the initial ED Triage tracing — and — on the baseline ECG from 1 year earlier. These are the 2nd and 3rd tracings shown above in the discussion by Drs. Hambright and Meyers — which I've reproduced and put together in Figure-1.
  • Because of its suboptimal resolution — it is much more difficult to compare the prehospital EMS tracing with the baseline ECG in today's case. Given that my reading of the prehospital EMS tracing is virtually the same as the initial Triage ECG (with the exception of there being some PVCs on the EMS tracing) — I think for educational purposes, it is reasonable to think of the “presenting ECG” as this initial ED Triage Tracing ( = ECG #2)

Figure-1: Comparison of the initial ED Triage Tracing — with this patient’s “baseline” ECG from 1 year earlier (See text).


What Do I Mean by a "Qualitative" Approach?
While the initial ED Triage Tracing ( ECG #2) by itself is not diagnostic for acute OMI — "qualitative" assessment of ST-T wave morphology is suspicious for an acute evolving event. 
  • As helpful as modified-Smith-Sgarbossa Criteria can be — I like to look for ST-T wave changes that I know are not normal in a patient with LBBB. These changes in ECG #2 are subtle — but they are present:
  • Since measurements are not used in the qualitative approach — I fully acknowledge that this approach is experiential. That said — this approach has consistently worked well for me over many years.
  • Since ST-T wave changes with the qualitative approach may be subtle — the more leads showing abnormal ST-T wave morphology — the greater the likelihood of an acutely ongoing cardiac event.

  • KEY Point: The best way to improve on recognition of subtle ST-T wave abnormalities in the setting of LBBB — is to routinely go back and compare the initial ECG of each case you encounter, with follow-up tracings obtained after acute reperfusion.

  • For More on the "Qualitative" Approach — Please check out My Comments in the September 17, 2020 post — the April 7, 2019 post — and the May 24, 2019 post in Dr. Smith's ECG Blog.

What Do We See in ECG #2 ( = the initial ED Triage Tracing)?
The rhythm in ECG #2 is sinus at ~60/minute. There is low voltage in the limb leads. The PR interval is prolonged (~0.24 second) — and the QRS complex is wide, consistent with complete LBBB.
  • Although difficult to assess because of the low voltage — there is straightening of the ST segment takeoff in each of the inferior leads (slanted BLUE lines in these leads)
  • Similar straightening of the ST segment takeoff is noted in lead V5. Note the subtle difference in shape of these "straightened" ST segments — compared to the gentle upsloping (normal) shape of the ST segment in leads V3 and V4 of ECG #2.

  • Normally with LBBB — lateral leads (ie, leads I,aVL,V6) manifest a depressed ST-T wave. It is not "usual" to see the amount of terminal T wave positivity highlighted by BLUE arrows in these leads. Again — there is low voltage in these lateral leads, which makes assessment of proportionality especially challenging. But I thought the relative size of the terminally upright T waves in leads I,aVL,V6 of ECG #2 was clearly more than I would normally expect.

To EMPHASIZE:
The above ST-T wave "qualitative" findings are subtle! These changes are not diagnostic of OMI! I was in NO way certain from this single initial ECG that an acute ongoing event was occurring. I would not activate the cath lab for these findings. That said:
  • This patient who presented with new chest pain is high-risk for having an acute event given his known history of coronary disease — and — his sudden onset of new symptoms severe enough to prompt EMS delivery to the ED. As a result — we need to lower our "threshold" for identifying ECG findings of concern.

  • Although subtle (and not diagnostic) — I thought suspicious ST-T wave findings were present in no less than 7/12 leads in ECG #2 (slanted BLUE lines and BLUE arrows in the Top tracing in Figure-1).

  • BOTTOM Line: Errors were made in the management of this case. The patient's chest pain was short-lived — and apparently resolving (if not resolved) by the time ECG #2 was obtained. The best way to tell IF the potentially concerning ST-T wave findings I identify above are real is with follow-up (ie, more than a single ECG in the ED — more than a single troponin in the ED — and being sure to correlate chest pain severity with the timing of serial ECGs and troponins). This was not done.

  • NOTE: If today's patient in fact had total coronary occlusion at the time he called EMS — and IF the reason his chest pain resolved (as his history suggests) at the time ECG #2 was recorded, was because there was spontaneous reperfusion of the "culprit" artery — then as per Drs. Hambright and Meyers, the reason frank ST elevation may not have been seen in ECG #2 — may have been because of "pseudonormalization" (ie, ST segments returning to the baseline on their way toward evolving inverted reperfusion T waves).

To Also EMPHASIZE:
My above interpretation was made before I looked at this patient's previous "baseline" ECG from 1 year earlier!
  • Seeing this patient's "baseline" tracing ( = ECG #3) — provides confirmation that the ST-T findings that I highlighted in BLUE in ECG #2 were all new compared to this patient's ECG 1 year earlier.
  • Terminally positive T waves were present in leads I and aVL of ECG #3. That said — Considering low amplitude of the QRS complex in these leads — Isn't this terminal T wave positivity more marked in leads I and aVL of ECG #2?
  • Starting from the flat ST segments in the inferior leads and in lead V4 of ECG #3 — Is there any doubt about the change in ST-T wave appearance, with ST segment straightening in each of these inferior leads in ECG #2? Given the history of new chest pain — I now interpreted these changed ST-T waves as hyperacute until proven otherwise.

In Summary:
As per Drs. Hambright and Meyers — today's patient returned to the ED 5 days later because of recurrent chest pain. To underscore the Learning Points highlighted above:
  • Chances are that IF more than a single troponin would have been obtained on the initial ED visit — that a 2nd troponin would probably have been abnormal enough to prompt investigation (instead of sending the patient home).
  • I also suspect that IF another ECG would have been done in the ED — that the "pseudonormalization" phase that we are probably seeing in ECG #2 — may have given way to evolution of "tell-tale" reperfusion T waves.

  • Additional Learning Point: Qualitative assessment of ST-T wave changes in patients with LBBB and new symptoms can clue you in to an acutely evolving event before frank Smith-Sgarbossa Criteria are satisfied. To "hone" your ability to pick up these subtle findings — Compare the inferior leads in ECG #2 with the inferior leads in the 4th tracing shown above in the presentation by Drs. Hambright and Meyers (ie, the Triage ECG on 2nd presentation). Doing so should illustrate why I immediately suspected that there might be an ongoing acute inferior OMI from the inferior lead ST-T wave straightening in the LBBB tracing shown in ECG #2.


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