A woman in her 30s with several days of chest pain and an episode of altered mental status.

Written by Pendell Meyers, reviewed by Smith, Grauer, McLaren

A woman in her early 30s with history of diabetes had 2-3 days of gradual onset nonradiating chest pain with associated nausea, malaise, and shortness of breath. Then she had an "abrupt change in her mental status and became more somnolent and less responsive" at home in front of her family. Her family called EMS, who found the patient awake and alert complaining of worsening chest pain compared to the prior few days.

En route to the ED, they recorded this ECG and transmitted it, asking whether the cath lab should be activated:

What do you think?

There is sinus rhythm at just under 100 bpm. The QRS has high leftward voltage consistent with LVH more than simple healthy young voltage. There is large STE in V1-V3, as well as aVL. There is STD in V5-6, II, III, and aVF. The T waves are questionably hyperacute in V1-V4, but the QRS is also very tall and dramatic. We have very few cases of LVH with large voltage present simultaneously with anterior hyperacute T waves, but the concern is that this could be one of them. A baseline ECG would help greatly (available below).

The subtle LAD OMI vs. normal variant STE formula is not applicable due to the presence of inferior reciprocal STD and lateral STD, and because it was not trained on LVH patients. 

If you had erroneously applied the formula, it would be falsely reassuring due to the large QRS voltage present in this case:

A prior baseline was available (though I doubt it was at hand when EMS asked for a prehospital decision on the ECG above):

Baseline (assuming baseline, no clinical info available) from last year.

With the baseline (just LVH with some normal variant STE), it is obviously easy to see that the initial ECG above is LAD OMI.

Here is her ECG immediately on arrival to the ED:

Obvious STEMI(+) OMI.

An ED echo reportedly showed an anterior wall motion abnormality and grossly depressed EF.

"Given patient's change in mental status, CTA of the chest was ordered to rule out dissection." 

Meyers note: I think CT angio for dissection is unnecessary in this case, as it is in almost all OMI cases. As Jesse McLaren pointed out to me, STEMI or OMI secondary to dissection is very rare (https://pubmed.ncbi.nlm.nih.gov/28511806/), so looking for it in the absence of compelling reasons (eg focal neuro or pulse deficit) will just delay reperfusion (https://pubmed.ncbi.nlm.nih.gov/22534052/).

"While at CT scanner, the patient lost pulses and appeared to have polymorphic VT cardiac arrest, then she achieved immediate ROSC with one defibrillation."

The initial high sensitivity troponin I returned at 34 ng/L.

The CT showed no dissection.

She proceeded to cath where they found total thrombotic proximal LAD occlusion (see images below).

ECG hours after PCI:

Next day ECG:

Troponin peaked at 23,591 ng/L.

Cardiac MRI done 5 days later:

EF 35%. Severe hypokinesis of the entire septum, anterior wall, and distal/apical segments. No LV thrombus. 

Learning Points:

LVH can make OMI interpretation more difficult. It is rare to see high LVH voltage in the same leads as OMI. But this one is an excellent example.

The first troponin is minimal when the benefit of reperfusion is maximal.

Comparison to baseline, and serial ECGs, can make a difficult interpretation easy. 

Sudden syncope or "seizure" in sick patients should be assumed to be cardiac arrest until proven otherwise.

Young people and women have OMI, and like other populations they may have delayed recognition.

OMI always evolves on ECG, if you have the ECGs to see it.

Young Women do suffer from thrombotic coronary occlusion!!

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MY Comment by KEN GRAUER, MD (8/15/2022):

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I saw the initial tracing in today’s case ( = ECG #1) — knowing only that the patient was a woman in her 30s on her way to the ED. I presumed she must have been having chest pain — but didn’t know how worrisome the history was (or was not) for a new cardiac event. I focus my comment on this initial tracing — which for clarity I’ve reproduced below in Figure-1. My thoughts on this initial ECG were the following:

• The rhythm is sinus at ~90-95/minute. Intervals (QR, QRS, QTc) and the frontal plane axis are normal (about +20 degrees).
• QRS amplitudes are greatly increased — especially in the chest leads, where there is significant "lead overlap" of complexes.

Regarding Q-R-S-T Changes:

• There are small and narrow Q waves in lateral leads (I,aVL,V5,V6) — which are almost certain to be normal septal q waves.
• R wave progression is normal (with transition appropriately occurring between leads V2-to-V3).

The KEY Question is whether ST-T wave appearance in ECG #1 is (or is not) suggestive of an acute cardiac event.

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

Should the Cath Lab Be Activated?

As emphasized by Dr. Meyers — assessment of the initial ECG in today’s case was complicated by the presence of LVH. It is simply not common to see the picture of markedly increased QRS amplitude, in association with hyperacute T waves in the anterior leads.

• Dr. Meyers also emphasized that on occasion — finding a baseline tracing on the patient for comparison can be diagnostic. This was the case with today’s patient — as a quick comparison with the previous ECG left NO doubt that the chest lead ST-T wave peaking in ECG #1 was a new (and therefore acute) finding. Unfortunately, baseline ECGs are not always available at the time they are needed for initial triage decision-making of whether or not to activate the cath lab. So HOW to proceed?

I’d point out the following.

• There are many ECG criteria for the diagnosis of LVH. I list those that I favor in Figure-2 — and discuss in detail my approach to the ECG diagnosis of LVH at THIS LINK.
• Note addition of the patient’s age to the criteria I suggest in Figure-2. The reason for including age — is that younger adults often manifest increased QRS amplitudes on ECG without true chamber LVH. While there is no universally-agreed-upon discrete “maximal age dividing point” — I’ve found ~35 years of age to work well clinically in my experience over decades.
• 
  
• This number “35” facilitates recall — because, of the 50+ criteria for LVH in the literature — by far the most sensitive and specific criterion in my experience also involves the number “35” (ie, Sum of deepest S in V1 or V2 + tallest R in V5 or V6 ≥35 mm satisfies voltage criteria for LVH in adults ≥35 years of age).
• 
  
• Assessment of LVH in the pediatric population is problematic — because of the difficulty determining reliable diagnostic voltage criteria for each age group (complicated further by technical issues of ensuring precise chest lead electrode placement in these smaller body frame patients). As a result — I routinely refer to tables for assessing maximal expected amplitudes for each specific age group.
• 
  
• To “simplify life” when assessing for LVH in younger adults (ie, patients in their late teens, 20s and early 30s) — I’ve found over the years that reversing the number “35” provides a quick “ballpark” assessment criterion as to whether there is sufficient voltage on the ECG of a younger adult (ie, who is under 35yo) to qualify for “LVH” (ie, Sum of deepest S in V1 or V2 + tallest R in V5 or V6 ≥53 mm).

Figure-2: Criteria I favor for the ECG diagnosis of LVH. (NOTE: I’ve excerpted this Figure from My Comment at the bottom of the page in the June 20, 2020 post in Dr. Smith’s ECG Blog).

Is there Voltage for LVH in Figure-1?

The patient in today’s case was a woman in her 30s — therefore more likely to manifest increased QRS amplitude not necessarily the result of LVH. Given the challenge of confusing “amplitude overlap” in the chest leads of Figure-1 — I clarify the limits of QRS deflections by coloring the complexes in Figure-3.

• Note that even accounting for the fact that today’s patient is a younger adult — the 53 mm criterion threshold is attained, suggesting true voltage for LVH in this younger age group patient.
• 
  
• Remember: The ECG is an imperfect tool to assess LVH. If true chamber size is needed — then an Echo (which also provides information on cardiac function) is far superior to ECG for assessment of chamber enlargement. That said — “pre-ECG interpretation likelihood” for LVH is clearly increased in today’s patient because of longstanding diabetes.

Figure-3: I’ve colored the QRS complex in 5 of the chest leads — to illustrate the actual size of the QRS complex in each of these leads. The deepest S wave is in lead V2 ( = 27 mm, as shown in RED) + the tallest R wave in lead V5 ( = 27 mm, as shown in GREEN) exceeds 53 mm. Note that the S wave in lead V1 is also unusually deep ( = 26 mm) — and the R wave in lead V4 is of unknown amplitude, since it is cut off by the top of the ECG paper (See text).

A Final Look at the ECG in Figure-1:

I fully acknowledge that I was not at all certain from seeing the initial ECG in Figure-1 whether this patient was (or was not) having an acute event. Against an acute event was the following:

• The patient has LVH on ECG — and as we have mentioned, it is uncommon to see hyperacute anterior T waves in association with marked LVH. Among the types of benign repolarization variants is T wave peaking that is often surprisingly tall in anterior leads in which there are deep S waves.
• There is excellent R wave progression — with an extremely tall R wave in lead V3 (R wave amplitude is typically reduced when there is anterior OMI).
• The QTc is at most no more than minimally prolonged (whereas acute infarction often produces significant QTc prolongation).

On the other hand — In Favor of an acute event until proven otherwise are the following:

• Although the patient in today's case is a young adult — this woman in her 30s has diabetes mellitus (presumably for some period of time) — therefore she clearly is at greater risk of myocardial infarction at an earlier age.
• Even accounting for LVH — the T wave in anterior chest leads is taller than is usually expected. This is especially true in lead V3 — where the 15 mm tall T wave is nearly as tall as the R wave in this lead. The "shape" of LV "strain" when seen in anterior leads tends to be the mirror-image opposite of the slow downslope-faster upslope ST depression typically seen in leads V5,V6 with LVH. It would be unusual to see such a tall, pointed T wave with narrow base from LVH as we see in lead V3.
• Neighboring leads V2 and V4 also appear taller and pointier than is usually seen with either LVH or depolarization variants.
• Finally, while the ST-T wave may normally be negative in lead III when the QRS is predominantly negative — there usually is not the J-point depression seen in Figure-3 (RED arrow in lead III).

BOTTOM Line: This young woman in her 30s has diabetes mellitus — and presented with a history of "worsening chest pain". While I was uncertain from her initial ECG if an acute process was ongoing — the worrisome history and questionable ECG features described above combine to clearly merit diagnostic cath to clarify the anatomy.

• To Emphasize: Once the prior ECG became available for comparison — there no longer was any doubt that the ECG findings highlighted above were acute!

Inferior ST Elevation and Hyperacute T-waves, but Patient is Pain Free. What is going on?

A 60-something female presented with episodes of chest pain for the previous 2 days that lasted 20 to 30 minutes each.  On the day of presentation, her episode lasted much longer and she came to the emergency department.  In the ambulance, she was given nitro and her pain was relieved.  On arrival to the emergency department she was pain free.

What do you think?

Here is an ECG from 3 years prior

This is classic Wellens' pattern B morphology, and fits with the entire presentation.  

So it is Wellens' syndrome.  The ECG is so classic that when I saw the ECG on the system, I knew it was the full syndrome and wrote that "this patient would be pain free at this moment."  Then I confirmed that when I went to the chart.

See important description of Wellens' syndrome below.

The providers who saw the patient were concerned about inferior OMI due to the subtle STE in inferior leads, and STD in aVL.

How do we KNOW it is not active inferior OMI?  

1. The patient is completely pain free and 2. Such inferior STE, and even apparent hyperacute T-waves, are commonly reciprocal to anterior and high lateral reperfusion.

Here is a similar case: 

How do you explain these inferior hyperacute T-waves?

1 hour later:

Further evolution (deepening) of symmetric T-wave inversion in precordial leads

Angiogram:

Acute MI Non ST Elevation Myocardial Infarction .

Culprit is 90% stenosis in the proximal LAD .

After PCI:

2 days later

Wellens' syndrome 

Wellens' syndrome is a syndrome of Transient OMI (including transient STEMI) of the LAD, in which the ECG was not recorded at the time of the anginal pain, but only after sponaneous resolution of the pain, at which time the ECG shows reperfusion T-waves in the LAD distribution.  Pattern A = terminal T-wave inversion (biphasic); Pattern B shows deep symmetric T-wave inversion.  Wellens' syndrome also requires preservation of R-waves. 

Thus, in Wellens' syndrome, the patient is: 

1) Pain free after an episode of angina,

2) Has a typical T-wave inversion morphology (not all T-wave inversion is Wellens!!), 

3) Will have preserved R-waves

4) Will have evolution of the T-wave inversion, 

5) Will always have some rise and fall of troponin, 

6) Will have an OPEN artery OR good collateral circulation (the myocardium is perfused)

7) At high risk of re-occlusion (with pseudonormalization of T-waves if it occurs)

Such T-wave inversion also occurs in all the other coronary distributions.

See these posts for a variety of Wellens and mimics:

Wellens' syndrome (25 cases!)

LVH mimics Wellens

Pulmonary Embolism vs. Wellens

PseudoWellens due to Unstable Angina

Wellens' with 100% LAD but good collateral circulation

Wellens' in inferior or lateral leads

Posterior Reperfusion T-waves (Wellens' of the Posterior Wall manifesting large V2 T-waves)

Wellens' in Paced Rhythm

Wellens' in LBBB

Wellens' Syndrome - NOT (mimics)

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MY Comment, by KEN GRAUER, MD (8/12/2022):

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An appreciation of Wellens' Syndrome is a must in emergency care. The "beauty" of this clinical entity is 3-Fold: i) Awareness of what to look for in the History and in the ECG allows diagnosis within seconds (as per Dr. Smith's instant analysis in today's case); ii) Recognition of Wellens' Syndrome tells you the anatomy (ie, accurate prediction of a high-grade proximal LAD stenosis); and, iii) Recognition of Wellens' Syndrome prompts the need for timely cath and life-saving treatment. 

• In addition to today's case — we've posted numerous examples of Wellens' Syndrome on Dr. Smith's ECG Blog (See the June 28, 2018 post — and the December 14, 2018 post — to name just 2 instances).
•  
• Unfortunately, despite the above expert commentary by Dr. Smith in today's case — Wellens' Syndrome remains a misunderstood diagnosis by all too many healthy care providers.

The History of Wellens' Syndrome:

It's hard to believe that the original manuscript describing Wellens' Syndrome was published 40 years ago! As I contemplated today's case — I thought it would be insightful to go back to this original manuscript (de Zwaan, Bär & Wellens: Am Heart J 103: 7030-736, 1982):

• The authors (de Zwaan, Bär & Wellens) — studied 145 consecutive patients (mean age 58 years) admitted for chest pain, thought to be having an impending acute infarction (Patients with LBBB, RBBB, LVH or RVH were excluded). Of this group — 26/145 patients either had or developed within 24 hours after admission, a pattern of abnormal ST-T waves in the anterior chest leads without change in the QRS complex.
• I've reproduced (and adapted) in Figure-1 — prototypes of the 2 ECG Patterns seen in these 26 patients. Of note — all 26 patients manifested characteristic ST-T wave changes in leads V2 and V3.
• Most patients also showed characteristic changes in lead V4.
• Most patients showed some (but less) ST-T wave change in lead V1.
• In occasional patients — abnormal ST-T waves were also seen as lateral as in leads V5 and/or V6.
• 
  
• Half of the 26 patients manifested characteristic ST-T wave changes at the time of admission. The remaining 13/26 patients developed these changes within 24 hours after admission.
• 
  
• Serum markers for infarction (ie, CPK, SGOT, SLDH) were either normal or no more than minimally elevated.

ECG Patterns of Wellens' Syndrome:

The 2 ECG Patterns observed in the 26 patients with characteristic ST-T wave changes are shown in Figure-1:

• Pattern A — was much less common in the study group (ie, seen in 4/26 patients). It featured an isoelectric or minimally elevated ST segment takeoff with straight or a coved (ie, "frowny"-configuration) ST segment, followed by a steep T wave descent from its peak until finishing with symmetric terminal T wave inversion.
• Pattern B — was far more common (ie, seen in 22/26 patients). It featured a coved ST segment, essentially without ST elevation — finishing with symmetric T wave inversion, that was often surprisingly deep. 

Figure-1: The 2 ECG Patterns of Wellens' Syndrome — as reported in the original 1982 article (Figure adapted from de Zwaan, Bär & Wellens: Am Heart J 103:730-736, 1982).

ST-T Wave Evolution of Wellens' Syndrome:

I've reproduced (and adapted) in Figure-2 — representative sequential ECGs obtained from one of the patients in the original 1982 manuscript.

• The patient whose ECGs are shown in Figure-2 — is a 45-year old man who presented with ongoing chest pain for several weeks prior to admission. His initial ECG is shown in Panel A — and was unremarkable, with normal R wave progression. Serum markers were negative for infarction. Medical therapy with a ß-blocker and nitrates relieved all symptoms.
•  
• Panel B — was recorded 23 hours after admission when the patient was completely asymptomatic. This 2nd ECG shows characteristic ST-T wave changes similar to those shown for Pattern B in Figure-1 (ie, deep, symmetric T wave inversion in multiple chest leads — with steep T wave descent that is especially marked in lead V3).
• 
  
• Not shown in Figure-2 are subsequent ECGs obtained over the next 3 days — that showed a return to the "normal" appearance of this patient's initial ECG (that was shown in Panel A of Figure-2). During this time — this patient remained asymptomatic and was gradually increasing his activity level.
• 
  
• Panel C — was recorded ~5 days later, because the patient had a new attack of severe chest pain. As can be seen — there is loss of anterior forces (deep QS in lead V3) with marked anterior ST elevation consistent with an extensive STEMI. Unfortunately — this patient died within 12 hours of obtaining this tracing from cardiogenic shock. Autopsy revealed an extensive anteroseptal MI with complete coronary occlusion from fresh clot at the bifurcation between the LMain and proximal LAD.

Figure-2: Representative sequential ECGs from one of the patients in the original 1982 article. Panel A: The initial ECG on admission to the hospital; Panel B: The repeat ECG done 23 hours after A. The patient had no chest pain over these 23 hours. NOTE: 3 days after B — the ECG appearance of this patient closely resembled that seen in A ( = the initial tracing). Panel C: 5 days later — the patient returned with a new attack of severe chest pain. As seen from this tracing (C) — this patient evolved a large anterior STEMI. He died within hours from cardiogenic shock (Figure adapted from de Zwaan, Bär & Wellens: Am Heart J 103:730-736, 1982 — See text).

Relevant Findings from the 1982 Article:

The ECG pattern known as Wellens' Syndrome was described 40 years ago. Clinical findings derived from the original 1982 manuscript by de Zwaan, Bär & Wellens remain relevant today.

• One of the 2 ECG Patterns shown in Figure-1, in which there are characteristic anterior chest lead ST-T wave abnormalities — was seen in 18% of 145 patients admitted to the hospital for new or worsening cardiac chest pain.
• Variations in the appearance of these 2 ECG patterns may be seen among these patients admitted for chest pain. Serial ECGs do not show a change in QRS morphology (ie, no Q waves or QS complexes developed). Serum markers for infarction remain normal, or are no more than minimally elevated.
• Among the subgroup of these patients in this 1982 manuscript who did not undergo bypass surgery — 75% (12/16 patients) developed an extensive anterior STEMI from proximal LAD occlusion within 1-2 weeks after becoming pain-free.

LESSONS to Be Learned:

At the time the 1982 manuscript was written — the authors were uncertain about the mechanism responsible for the 2 ECG patterns of Wellens' Syndrome.

• We now know the mechanism. A high percentage of patients seen in the ED for new cardiac chest pain that then resolves — with development shortly thereafter of some form of the ECG patterns shown in Figure-1 — had recent coronary occlusion of the proximal LAD — that then spontaneously reopened.
• 
  
• The reason Q waves do not develop on ECG and serum markers for infarction are normal (or at most, no more than minimally elevated) — is that the period of coronary occlusion is very brief. Myocardial injury is minimal (if there is any injury at all).
• 
  
• What spontaneously occludes — and then spontaneously reopens — may continue to reocclude, and then reopen — until eventually a final disposition is reached (ie, with the "culprit" vessel staying either open or closed).
• 
  
• As per the above discussion by Dr. Smith — We can know whether the "culprit" artery is either open or closed by correlating serial ECGs with the patient's history of chest pain. For example, in today's case — the finding of deep, symmetric T wave inversion in virtually all chest leads in association with resolution of the chest pain immediately told Dr. Smith that the LAD had spontaneously reopened.
• 
  
• The importance of recognizing Wellens' Syndrome — is that it tells us that timely cardiac cath will be essential IF we hope to prevent reclosure. In the de Zwaan, Bär & Wellens study — 75% of these pain-free patients with Wellens' ST-T wave changes went on to develop a large anterior STEMI within the ensuing 1-2 weeks if they were not treated.
• Thus, the goal of recognizing Wellens' Syndrome — is to intervene before significant myocardial damage occurs (ie, diagnostic criteria for this Syndrome require that anterior Q waves or QS complexes have not developed — and serum markers for infarction are no more than minimally elevated).
• It is not "Wellens' Syndrome" — IF the patient is having chest pain at the time the ECG patterns in Figure-1 are seen. Active chest pain suggests that the "culprit" artery has reoccluded.
• Exclusions from the 1982 study were patients with LBBB, RBBB, LVH or RVH. While acute proximal LAD occlusion can of course occur in patients with conduction defects or chamber enlargement — Recognition of the patterns for Wellens' Syndrome is far more challenging when any of these ECG findings are present.
• 
  
• Finally — a word about the ECG Patterns of Wellens' Syndrome shown in Figure-1 is in order. Pattern A — is far less common, but more specific for Wellens' Syndrome IF associated with the "right" history (ie, prior chest pain — that has now resolved at the time ST-T wave abnormalities appear).
• Unlike the example in Figure-1 — Pattern B may be limited to symmetric T wave inversion without the finding of steep T wave descent into terminal negativity in any lead. This is the pattern seen in today's case — which given the history, was immediately diagnosed as Wellens' Syndrome by Dr. Smith.

In Conclusion — the 145 pts studied by de Zwaan, Bär & Wellens in 1982 continue to provide clinical insight into the nature of Wellens' Syndrome some 40 years after this manuscript was written.

• P.S.: And sometimes — there may be a similar evolution of ECG findings indicative of acute occlusion and spontaneous reperfusion (corresponding to changes in chest pain severity) in not only anterior leads — but also in the inferior leads. As per Dr. Smith in today's case — this is not active acute inferior OMI — but rather a "reciprocal part" of the Wellens' Syndrome evolution.

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):

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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.