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

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

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

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

Here is the initial ECG at 1723:

What do you think? 

Annotated with J points identified in all leads

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

Here is a normal (baseline) RBBB for reference:

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

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

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

The second troponin I resulted at 84 ng/L.

Another ECG was recorded at 1759:

I do not see much change. The STE in V4 is slightly greater.

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

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

Right sided leads were recorded at 2010:

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

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

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

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

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

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

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

Discussion:

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

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

References:

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

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

Nikparvar, M., Asghari, S. M., & Farshidi, H. (2019). Delayed diagnosis of myocardial infarction in a young man with a blunt chest trauma. Journal of cardiovascular and thoracic research, 11(3), 251–253. 

A 50 year old man with sudden altered mental status and inferior STE. Would you give lytics? Yes, but not because of the ECG!

Submitted by Alex Bracey, written by Pendell Meyers

A man in his 50s was hunting with a friend when he suddenly "fell out" (similar to syncope), but then did not return to baseline, and instead had persistent altered mental status. His friend was able to get him into the truck and drive him to a nearby community hospital (non-PCI center). 

When he arrived, his mental status had deteriorated further, to the point that he was quickly intubated on arrival. After intubation, vital signs were all within normal limits. He was quickly rushed to the CT scanner and a noncontrast head CT was completely normal.

Side note: The differential of sudden persistent loss of consciousness with adequate hemodynamics is relatively short: seizure, intracranial hemorrhage, basilar artery occlusion. After a negative noncontrast head CT the next step is looking for a hyperdense basilar artery sign AND to perform a CT cerebral angiogram).

An ECG was recorded quickly on return to the ED:

(sorry for poor quality, cannot get originals)

What do you think?

There is a narrow complex regular rhythm at a rate of approximately 120 bpm. There is the appearance of STE in inferior leads II, III, and aVF (with STD in aVR), but this is entirely due to flutter waves which are only seen in those leads. 

Also, the atrial flutter in this case is relatively slow like in many other cases we've shown. Normal atrial size and conduction rate typically results in a flutter circuit of about 300 bpm, with 2:1 conduction causing resultant ventricular rate of about 150 bpm. Here the flutter rate is approximately 240 bpm, with ventricular rate around 120 bpm. This implies a large atrium, slowed conduction (due to, for instance, Na channel blocking agents), or both.

We have shown countless examples of this same phenomenon (atrial flutter mimicking inferior STE or STD). We have also shown several cases in which atrial flutter hides true, active ischemia.

Christmas Eve Special Gift!! Prehospital Cath Lab Activation: What do you think?

Global ST depression with ST elevation in aVR - what is the cause?

Is this inferor STEMI?

Tachycardia and ST Elevation.

Atrial Flutter with Inferior STEMI?

Atrial Flutter Mimicking ST Depression

What is the Diagnosis?

Inferolateral ST elevation, vomiting, and elevated troponin

The treating team did not identify the flutter waves and they became worried about possible "STEMI" (despite the unusual clinical scenario). They called their transfer center cardiologist on call, who reviewed the case on the phone with them, as well as the ECG. The EM provider asked if the cardiologist thought it was a "STEMI." The cardiologist also did not see atrial flutter, and advised giving thrombolytics for perceived "inferior STEMI."

The patient received thrombolytics and then was transferred to the PCI referral center. 

On arrival to the PCI center's Emergency Department, the receiving team recorded an ECG on arrival:

Persistent atrial flutter, however this time the QRS occurs on a slightly different portion of the flutter wave. In my opinion this makes the flutter waves slightly easier to recognize in this ECG.

Atrial flutter was recognized at this time. On arrival, apparently the patients mental status was improved compared to his initial presentation, because he was noticed to be pulling at his tube and gagging, requiring sedation.

The case was reviewed by the receiving team who had concerns for acute stroke or other cause of acute altered mental status. 

A CT angiogram of the head and neck was performed which showed a basilar artery thrombus which was concerning for brainstem stroke as the inciting cause. There was again no intracranial hemorrhage. Serial troponins were negative. 

The patient was admitted for stroke management. No obvious adverse events were attributed to the thrombolytics. Long-term outcome is unknown.

Thus, it seems that two mistakes may have inadvertently led accidentally to the appropriate administration of thrombolytics!! They mistook atrial flutter for STEMI, and did not recognize the clinical presentation of basilar artery occlusion. Correct, but for the wrong reason!

So the answer to the title of this post is: "Yes, I have a patient with a devastating stroke, and I do not have neurointerventional capabilities, so I will give thrombolytics!"

Discussion

Flutter waves are well known to mimic ST deviations, as well as to hide true ischemic ST deviations from the interpreter. In many cases of flutter waves mimicking ST deviations, the expert electrocardiographer can see the morphology of the flutter waves as the cause of apparent STE or STD. Likewise, in some cases of ischemia concealed by flutter waves, the ischemia can be seen despite the flutter waves, whereas in other cases the dysrhythmia must be terminated before the ischemia can be clearly distinguished. 

Even when flutter waves conceal true ST segment deviations, the cause and effect relationship may be unclear. Tachycardia to this degree can cause ST segment changes in several ways. First, there can simply be diffuse STD (which obligates reciprocal STE in aVR) associated with tachycardia, which are not even necessarily indicative of ischemia. Second, the increased demand created by extreme tachycardia may exceed the ability of the coronary arteries to supply sufficient blood (due to preexisting three vessel or left main disease, with or without ACS). In this case, there is diffuse ischemic STD of subendocardial ischemia, of course with accompanying reciprocal STE in aVR. Finally, if a region of the myocardium supplied y a severely flow-limiting (but not necessarily fully occluded) lesion suddenly undergoes massively increased demand due to acute tachycardia, the supply-demand mismatch may be so great that the tissue undergoes acute transmural ischemia, both subendocardial and subepicardial, which may result in infarction (just as in the case of classic thrombotic occlusion MI). This case represents the same physiologic event as OMI in terms of the result on the myocardium, therefore with identical ECG features, however, ACS may not even be present.

ST Depression Maximal in V1-V4 and Angio shows 3 Vessel Disease. Is it posterior? Which is the culprit?

A 70-something woman had acute chest pain.

The ECG was texted to me with the words: "Acute chest pain. Could this be posterior MI? What do you make of the ST depression in V4-V6?"

What do you think?

My response: "The ST depression is maximal in V1-V4.  This is most consistent with a posterior MI.  If it sounds clinically like acute MI then this is good for activating the cath lab."

Her response: "Yeah, I did activate.  But the cardiology fellow told me he was sure it would not be a posterior MI because of diffuse ST depression.  He suggested that we should have consulted cardiology rather than activating the cath lab, and treated this like a NonSTEMI."

My response: "That is not true.  It is possible that it is not posterior, but about 80-90% of the time it is posterior if the STD is maximal in V1-V4.  So if it turns out not to be, that does not mean he was right.  He was not right."

She did give nitroglycerine, and the pain improved but did not resolve, then recorded this ECG:

The ST depression persists but is not as profound

I did not know this at the time, but because of a widened mediastinum on CXR, they did a CT aortogram that was negative (I use one CT image below to illustrate "posterior" MI).

The first troponin I returned at 4100 ng/L -- quite high for a very acute MI, usually seen in subacute MI.

Angiographic findings (done approximately 150 minutes after 1st ECG):

Brisk, TIMI III flow into all coronaries. Severe distal vessel tortuosity and moderate left coronary calcium.

1. Left main: normal.

2. LAD: Type III. Long (~35 mm) moderately calcified 70% proximal to mid LAD stenosis.

      A diagonal branch distal to the stenosis has luminal irregularities.

3. LCX: Tortuous, mildly calcified with luminal irregularities in the proper vessel and a 80-90% stenosis in the proximal OM followed by a 70% stenosis downstream after two 90 degree bends. A smaller OM has luminal irregularities. 

4. RCA: Long (>35 mm), 70% mid RCA stenosis stenosis. It supplies a medium sized RPDA and small RPLA 

So there is severe 3 vessel disease, but all arteries are open with good flow.  This seems to imply that the fellow was correct in this case, but this is not true.  The arteries were clearly not all widely patent (open) at the time of ECG recording, 150 minutes earlier.  Spontaneous reperfusion with TIMI-3 (normal) flow is very common, occurring in up to 19% of proven STEMI (1).  When there is such full reperfusion of an occlusion (OMI), it makes it difficult to identify the culprit on angiogram unless there is clearly an ulcerated plaque on the angiogram, which apparently there was not, or the angiographer would have found it.

However, had the angiogram been done at exactly the same time as the first ECG, the culprit would have been apparent.

The fact that the proximal OM (obtuse marginal branch off the circumflex) had such a tight stenosis makes it a likely culprit for the acute plaque rupture, but not certain.

Furthermore, the arteries were "tortuous" (full of twists and turns) and so any PCI was going to be technically difficult, so it was deferred at that point in order to discuss Coronary Bypass surgery (CABG).

The troponin peaked over 21,000 ng/L. This is very high and a level more consistent with STEMI/OMI than with NonSTEMI, although there is quite a bit of overlap.  Most STEMI have troponin I over 10 ng/mL (roughly equivalent to 10,000 ng/L), and most NonSTEMI have troponin I below 10 ng/mL.  

The formal bubble contrast echocardiogram: "Findings are most consistent with ischemia/infarct in the diagonal and OM vascular territories."  This confirms Posterior MI.

The patient refused Bypass Surgery (CABG), and so was taken back for another angiogram and intervention.

2nd angiogram, with intervention:

Culprit Lesion (s): 80% stenosis of proximal OM1 in the setting of significant tortuosity.  Successful PCI of proximal OM stenosis.

All subsequent ECGs continued to have ST depression (not shown), suggesting a No Reflow phenomenon.  No further troponins were measured.

Learning points:

1. Precordial ST Depression, when maximal in V1-V4 (vs. V5-V6) is reciprocal to ST Elevation in the wall opposite those leads (i.e, posterior wall, which is now often and confusingly called "Lateral" -- see below) and indicates posterior OMI in 80-90% of cases.

2. Diffuse ST depression, maximal in II, V5 and V6 is more often due to diffuse subendocardial ischemia and has reciprocal ST Elevation in aVR.

3. Even when there is 3-vessel disease, one of them is usually the acute culprit, whether it can be identified or not.  Intervening can be hazardous however, which is one reason that CABG is often recommended.

4. 15-20% of OMI are reperfused by the time of the ECG.  A very high troponin (TnI over 10.0 ng/mL or 10,000 ng/L; TnT over 1.0 ng/mL or 1000 ng/L) can help to ascertain whether there was occlusion at the time of the ECG.  This is a crucial part of our ECG research -- when we assess the ECG, we need to figure out what the state of the artery was during its recording.

5. Echocardiogram can help to determine if precordial ST depression is due to subendocardial ischemia (absence of wall motion abnormality, or at least not in posterior location) vs. posterior (posterior or lateral WMA).

6.  Posterior MI is now frequently called "Lateral" (see articles by Bayes de Luna below).  I prefer the old terminology of "Posterior" (see image and explanation below) because it differentiates OMI with ST depression ONLY (V1-V4) from OMI that has ST Elevation, with or without ST depression.  See this:

This is the CT scan image of this patient

The area of transmural infarct is outlined in red.

It is the lateral wall.

--However, due to rotated orientation in the chest, the lateral wall of the heart is oriented towards the posterior thorax, directly opposite V1, V2, and V3.

--Posterior leads V7-V9 would have shown STE if the voltage was high enough.  

--All that lung between the heart and V7-V9 can result in insufficient QRS or ST-T voltage!

--V1-V3 are directly opposite the wall with STE (under leads V7-V9), and therefore show reciprocal ST Depression.

--Therefore, it is more appropriate to call this a posterior STEMI than a "lateral" STEMI.

--A lateral STEMI would show STE on the 12-lead in V5 and V6 (or high lateral in I, aVL)

1. Cox DA, Stone GW, Grines CL, et al. Comparative Early and Late Outcomes After Primary Percutaneous Coronary Intervention in ST-Segment Elevation and Non–ST-Segment Elevation Acute Myocardial Infarction (from the CADILLAC Trial). Am J Cardiol [Internet] 2006;98(3):331–7. Available from: http://www.sciencedirect.com/science/article/pii/S0002914906007168

Articles by Bayes de Luna which attempt to eliminate the idea of a "Posterior MI".  

I find that these ideas only confuse the acute treatment of any Occlusion MI (OMI) that only manifests ST depression in leads V1-V4.  By propagating the idea that there is no posterior MI, they propagate the idea that patients who do not have ST Elevation do not have OMI (or STEMI equivalent with ST Elevation vector pointing towards the posterior thorax).

… R wave in V₁ is caused by a lateral not posterior myocardial infarction—new evidence based on contrast-enhanced cardiac magnetic resonance—electrocardiogram …

A Bayés de Luna, D Rovai, G Pons Llado… - European Heart …, 2015 - academic.oup.com

Paperpile

Since 1964, a tall and broad R wave in V1–V2, in the absence of right ventricular
hypertrophy, complete right bundle-branch block, or Wolff–Parkinson–White syndrome, has
been considered the sign of a posterior myocardial infarction (MI). 1 According to this theory … Cited by 21 Related articles All 10 versions Import into BibTeX

Concordance of electrocardiographic patterns and healed myocardial infarction location detected by cardiovascular magnetic resonance

AB de Luna, JM Cino, S Pujadas… - The American journal of …, 2006 - Elsevier

Paperpile

Q-wave myocardial infarction (MI) location is generally based on a pathologic correlation
first proposed> 50 years ago. Despite the proved reliability of contrast-enhanced
cardiovascular magnetic resonance (CE-CMR) imaging to detect and locate infarcted areas  Cited by 84 Related articles All 7 versions Import into BibTeX

[HTML] ahajournals.orgFull View

A new terminology for left ventricular walls and location of myocardial infarcts that present Q wave based on the standard of cardiac magnetic resonance imaging: a …

A Bayes de Luna, G Wagner, Y Birnbaum, K Nikus… - Circulation, 2006 - Am Heart Assoc

Paperpile

The ECG is the most frequently used tool for evaluating myocardial infarction (MI). The ECG
provides an opportunity to describe location and extent of infarction expressed as
pathological Q waves or their equivalents. The terminology used for the left ventricular (LV) …

 

Bradycardia, Crushing Chest pain, and Pulseless VT Arrest

A 50-something woman with h/o hypertension and hyperaldostonism presented with severe crushing chest pain and bradycardia.  EMS found the patient with a decreased level of consciousness.  En route to the ED, the heart rate was 30-60 with systolic BP in the 150s and the patient was talking and answering questions.  

They recorded a prehospital ECG:

What do you think?

The patient arrived awake and had another ECG recorded:

What do you think?

The ED physicians correctly identified hyperkalemia and pseudoSTEMI (bradycardia, STE in V1 and V2, very peaked T-waves with a narrow bse and very flat (even downsloping) ST segment.  They gave 3 g of calcium gluconate immediately.  They then noted ventricular tachycardia on the monitor.  The patient was unresponsive and pulseless.  

After appropriate resuscitative measures and treatment for hyperkalemia, including lots of calcium, ROSC was obtained.

The K returned at 8.7 mEq/L. 

Here is the post resuscitation ECG:

Almost totally normal High Sensitivity Trop peaked at 143 ng/L (not terribly high for cardiac arrest & not high enough to support diagnosis of true STEMI as explanation for her chest pain, ST Elevation, and cardiac arrest).

Learning Point

1. Although arrest from hyperkalemia is most commonly due to widening, sine wave, and PEA, it can definitely cause VT/VF arrest.  

2. Hyperkalemia causes a pseudoSTEMI pattern in V1 and V2, in addition to other well known findings.

1. Case of hyperK and VT in which I gave 15 g of calcium gluconate before the VT would stop.

Weakness, prolonged PR interval, wide complex, ventricular tachycardia

2. Case of HyperK that looks like early repol that resulted in ventricular fibrillation (see Case 3 in this post):

HyperKalemia with Cardiac Arrest. Peaked T waves: Hyperacute (STEMI) vs. Early Repolarizaton vs. Hyperkalemia

A woman with near-syncope, bradycardia, and hypotension

 Written by Pendell Meyers

A 59-year-old woman with diabetes, hypertension, prior stroke, and peripheral vascular disease presented with multiple near-syncopal events over the past 2 days, as well as ongoing back pain. EMS found her bradycardic in the 40s and administered atropine with no response. She was mentating and had a reasonable blood pressure (around 90s systolic), so they decided not to pace prehospital.

 

On arrival the patients blood pressure was 79/50 mm Hg. She was still awake and alert. Here is her first ECG (no baseline available):

What do you think?

Findings:

 - junctional bradycardia (no P waves, slow regular QRS rhythm, QRS is slightly wide [computer 119ms] but not wide or disorganized enough to be ventricular in origin)

 - widened QRS (as above, must assume QRS widening is new until proven otherwise)

 - QRS with LAFB morphology

 - Peaked T waves in V2-V5

Interpretation:

Diagnostic of severe hyperkalemia. No evidence of inferior OMI (which should always be scrutinized for to explain sick bradycardia, because the RCA usually supplies the SA and AV nodes).

The provider read this as a junctional bradycardia. There was no initial recognition of hyperkalemia. Dopamine was started as well as a fluid bolus, yet the heart rate was still in the high 30s. Cardiology was called emergently for advice as to whether they should start pacing.

The labs returned in time to show a potassium level of 7.1 mEq/L before pacing was performed.

She received calcium, insulin, dextrose, and lasix. The heart rate and blood pressure were reported to improve within minutes of calcium, however no ECG is recorded at that time. Further labs revealed acute renal failure. 

She had no further hemodynamic instability, and she was admitted.

The next morning her labs showed a potassium concentration of 4.5 mEq/L. Here is her ECG around that time:

Much improved. Sinus rhythm. QRS slightly narrower (computer says 110 ms), but LAFB morphology appears to be baseline. The T waves are still slightly peaked.

Learning Points:

Remember the "Killer B's" of hyperkalemia: Brady, Broad, Blocks, and Bizarre. These findings are associated with especially high risk of deterioration and cardiac arrest from hyperkalemia (peaked T waves less so, but do not be reassured). This patient has 2/4 (bradycardia and widening of the QRS complex).

Hyperkalemia treatment likely prevented cardiac arrest in this patient, and it could have been recognized and treated sooner.

Emergency medicine providers have to be the experts on acute severe hyperkalemia, and the ECG is the key to mastering this.

Never pace a patient without first considering calcium and hyperkalemia.

Extreme widespread ST depression, with ST Elevation in aVR. What do you think?

 I was texted this ECG without any other information.  The question was posed: "Activate the cath lab?"

What do you think?

What was my answer?

There is diffuse ST depression due to widespread severe subendocardial ischemia.  The ST elevation in aVR is reciprocal to that ST depression.

Smith answer: "Of course there is severe ischemia.  But the question is: Is it due to acute coronary syndrome?  What is the clinical situation?"

Clinical history

This is a young homeless intravenous drug user who presented with chest pain, nausea and vomiting, chills and a left foot wound.  He was hypothermic with a blood pressure of 98/19.  

What do you think now?

With the wide pulse pressure and extremely low diastolic pressure, aortic regurgitation (insufficiency), probably from endocarditis, was immediately suspected and confirmed with bedside echo with doppler.  Other etiologies of low diastolic pressure and high pulse pressure include anything that causes severely decreased systemic vascular resistance, though few such entities are this profound.  

Remember that the coronaries are perfused by diastolic aortic pressure. During systole, the LV intraventricular pressure is high and prevents perfusion. (The exception is the right ventricular coronary branches, which are perfused in systole as well because RV pressure is lower than systolic pressure).  Aortic regurgitation greatly decreases diastolic aortic pressure, and increases diastolic LV pressure, so that there is very little flow in the coronaries with such a low diastolic pressure, and the worst location of that ischemia will be adjacent to the LV cavity, which is the subendocardium.

In spite of maximal medical therapy and planning for immediate surgery, the patient died.

This case was obviously not ACS, and my partners knew it all along.  They just wanted to see what my reaction to the EKG would be.

Learning point

Most widespread ST depression, with STE in aVR is NOT due to ACS.  See 2 papers referenced below.

The differential diagnosis for widespread ST depression with STE in aVR is anything that can cause supply demand mismatch.  So anything that   Some important ones are listed here:

1. Valvular disease

2. Severe anemia

3. Severe hypoxia

4. Hypotension, especially diastolic hypotension

5. Hemoglobinopathies or cellular toxins

6. Severe LVH or HOCM, which prevents adequate perfusion

7. Extreme tachycardia

8. Extreme hypertension

9. Lesser degrees of any of the above, if combined with fixed coronary stenoses.

Acute coronary syndrome.  Severe Left Main stenosis (not occlusion!) or LAD, or single vessel ACS with 3 vessel disease.

The ECG does not differentiate the above etiologies, it simply signifies that there is severe diffuse global supply-demand mismatch, whatever the etiology.

LVH, LBBB, RBBB, and RVH may manifest ST depression without any ischemia

Other cases:

Aortic Stenosis:

Diffuse Subendocardial Ischemia on the ECG. Left main? 3-vessel disease? No!

An elderly man with sudden cardiogenic shock, diffuse ST depressions, and STE in aVR

Literature

1. Knotts et al. found that such ECG findings (STE in aVR) only represented left main ACS in 14% of such ECGs: 

Only 23% of patients with the aVR STE pattern had any LM disease (fewer if defined as ≥ 50% stenosis). Only 28% of patients had ACS of any vessel, and, of those patients, the LM was the culprit in just 49% (14% of all cases).  It was a baseline finding in 62% of patients, usually due to LVH.

Reference: Knotts RJ, Wilson JM, Kim E, Huang HD, Birnbaum Y. Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? J Electrocardiol 2013;46:240-8.

2.  Now there is a paper published in 2019 that proves the point beyond doubt, though makes it clear that this pattern is associated with very high mortality.

https://www.sciencedirect.com/science/article/abs/pii/S000293431930049X
Harhash AA et al. aVR ST Segment Elevation: Acute STEMI or Not? Incidence of an Acute Coronary Occlusion.  American Journal of Medicine 132(5):622-630; May 2019.

Here is the abstract:

Background

Identification of ST elevation myocardial infarction (STEMI) is critical because early reperfusion can save myocardium and increase survival. ST elevation (STE) in lead augmented vector right (aVR), coexistent with multilead ST depression, was endorsed as a sign of acute occlusion of the left main or proximal left anterior descending coronary artery in the 2013 STEMI guidelines. We investigated the incidence of an acutely occluded coronary in patients presenting with STE-aVR with multi-lead ST depression.

Methods

STEMI activations between January 2014 and April 2018 at the University of Arizona Medical Center were identified. All electrocardiograms (ECGs) and coronary angiograms were blindly analyzed by experienced cardiologists. Among 847 STEMI activations, 99 patients (12%) were identified with STE-aVR with multi-lead ST depression.  

Smith comment: this is a very limited population, as it only includes those with STEMI activations.  There are likely many other patients with STE-aVR who did not get a STEMI activation as they were not suspected of having ACS.

Results

Emergent angiography was performed in 80% (79/99) of patients. Thirty-six patients (36%) presented with cardiac arrest, and 78% (28/36) underwent emergent angiography. Coronary occlusion, thought to be culprit, was identified in only 8 patients (10%), and none of those lesions were left main or left anterior descending occlusions. A total of 47 patients (59%) were found to have severe coronary disease, but most had intact distal flow. Thirty-two patients (40%) had mild to moderate or no significant disease. However, STE-aVR with multilead ST depression was associated with 31% in-hospital mortality compared with only 6.2% in a subgroup of 190 patients with STEMI without STE-aVR (p less than 0.00001).  

Comment: Again, this does not include the many STE-aVR patients who were not activated, so even fewer would have ACS, and mortality in this group is much greater than in all STE-aVR patients.

Conclusions

STE-aVR with multilead ST depression was associated with acutely thrombotic coronary occlusion in only 10% of patients. Routine STEMI activation in STE-aVR for emergent revascularization is not warranted, although urgent, rather than emergent, catheterization appears to be important.

A 45 year old smoker presents with palpitations, is discharged, and is found dead 2 days later

A 45 year old smoker presented with palpitations.  He had no other medical problems.  There was no syncope.  He was on no medications.

Unfortunately, no other information is available, but that is enough to provide an learning point.

Here is the EKG:

Do you see anything worrisome?

There are PVCs, and these might be the cause of the palpitations (whether they are indeed the source of the palpitations could easily be ascertained by asking the patient if the palpitations are still present during the ECG).  

However, there are wide QS-waves (0.8 ms) in III and aVF, and they have a fragmented QRS (extra spike in the middle of the Q-wave, down-up-down).  Fragmented QRS is defined as additional spikes within the QRS complex.  It is a sign of myocardial scar and a significant risk factor for serious dysrhythmia and sudden death.  

Although PVCs are not dangerous in the absence of other significant pathology, they are another clue that there may be myocardial scarring and PVCs are frequently the initiating stimulus for Ventricular Tachycardia (VT) and ventricular fibrillaton (VF) (and not only for polymorphic VT/Torsades). 

Clinical Course

The extent of the patient's ED evaluation was not provided.  

For instance, we don't know the character of the palpitations.  

"Was your heart beating fast?  Or just jumping around in your chest?"  

"Did you take you pulse during the palpitations?"  

"While the tech was recording your ECG, were you having the same symptoms?"  

"Did you feel as if you might pass out during the palpitations?"

"Was there shortness of breath or chest pain?"

In addition, electrolyte concentrations are not available, nor troponin.  But since he was discharged to home, let's assume they were normal.  

2 days later he was found dead.   No further details are available.

Although no details are available, it is a reasonable probability, or even high probability, that the patient suffered an arrhythmic death.  

In any case, it presents a learning opportunity.

The palpitations may have been ventricular tachycardia.  Myocardial scar, as evidenced by the inferior fragmented QRS, is a nidus for a primary ventricular dysrhythmia.  A recurrent dysrhythmia might be VF, or VT that degenerated into VF.

Palpitations.

Palpitations as an ED chief complaint are the subject of an upcoming study. According to another study, palpitations comprise about 0.6% of ED visits, 1/4 of which result in hospital admissions.  1/3 are given "cardiac diagnosis."  

Diagnoses associated with palpitations are many, though among those without syncope, they are mostly non life-threatening, and include PACs, PVCs, SVT, atrial fibrillation/flutter, pre-excited and Ventricular tachycardia.  Of course atrial fib is particularly important because it can lead to stroke.  Some of the abnormal rhythms are still present on arrival to the ED, some are terminated.  It is the ones that are terminated which are obviously most difficult to diagnose, unless there are telltale signs on the 12-lead ECG such as Brugada, long QT, WPW, RV dysplasia, or HOCM.  Ventricular tachycardia (VT) is the most dangerous of these (except for WPW with atrial fib).

VT is commonly caused by not only the above named syndromes, but by myocardial scar from many pathologies, but most commonly from ischemic cardiomyopathy, due to myocardial scarring from previous MI.  

Such scarring is not always evident on the ECG, or it may manifest pathologic Q-waves.  But QRS fragmentation is a sign of myocardial scarring, so for this patient the ECG risk is quite high.

When to hospitalize

This comes from: Management of patients with palpitations: a position paper from the European Heart Rhythm Association, in EuroPace (2011)

This patient would fall under "Primary electrical heart disease, suspected."  or "Severe structural heart disease, suspected."

In a patient with palpitations, Q-waves due to old infarction, especially those with a fragmented QRS should lead you to suspect structural heart disease and primary electrical heart disease.

Learning point

"Palpitations" is a common ED complaint and can usually be evaluated in the ambulatory setting unless associated with syncope (or perhaps presycope), or any of the above considerations (in the table).  If I saw such a patient with palpitations and a fragmented QRS, or even known previous myocardial infarction (MI) alone, (or also any patient with decreased LV function on point of care bedside echo), I would admit for further workup, which may include formal contrast echo, angiography, MRI, Stress testing, CT coronary angiography, or even electrophysiology study, depending on the cardiologist's evaluation.

More on Fragmented QRS

Free full text: Fragmented QRS for the prediction of sudden cardiac death: a meta-analysis

This paper found that a fragmented QRS in inferior leads is a particular high risk for sudden death: QRS fragmentation and the risk of sudden cardiac death in MADIT II

Fragmented QRS: a predictor of mortality and sudden cardiac death

Full text: Fragmented QRS: What Is The Meaning?

Here are more examples of fragmented QRS from previous posts, including Chapman's sign and Cabrera's sign in LBBB

H/o MI and stents with brief angina has this ED ECG. And what is Fractional Flow Reserve?

Sudden Chest pain and SOB with a Wide Complex Tachycardia

30-something with chest pain, a fragmented QRS, and ST Elevation.

CHF Exacerbation with Old LBBB: Is There New Infarction or Not?

Pericarditis, or Anterior STEMI? The QRS proves it.

Left Bundle Branch Block and Left Anterior Descending Artery occlusion: Serial ECGs then T-wave inversion after reperfusion