What would you do with acute chest pain and this ECG? You might see what the Queen thinks.

This is another case sent by the undergraduate (who is applying to med school) who works as an EKG tech.

Case

An 82 year old man with a history of hypertension presented to the ED with chest pain at 1211. He described his chest pain as pleuritic and reported that it started the day prior while swinging a golf club. 

An EKG for chest pain was obtained right away:

For an 82 year old, this is a good looking EKG, with sinus rhythm at a rate of 70 BPM.   

It is really completely normal

On arrival, the patient’s vital signs were normal and he rated the chest pain 1/10. A troponin T was drawn at 1229 and resulted slightly elevated at 23 ng/L (URL for men in this assay is 15 ng/L).

Three months prior to this presentation, he received a pacemaker for severe bradycardia and syncope due to sinus node dysfunction. 

The ED provider ordered a coronary CT scan to assess the patient for CAD. 

At around 1430, as the patient was being prepared to leave for the scan, he developed severe chest pain, dizziness, and became diaphoretic. Another blood pressure was checked. He was severely hypotensive, with a systolic pressure in the 50s. 

Another EKG was obtained:

There is now an atrial paced rhythm.  And there is significantly more ST Elevation.

Here is the PM Cardio digitization:

There are some notable changes between this EKG and the last. Most strikingly, there is new ST elevation most prominent throughout the proximal LAD distribution.

However, there is also a problem with digitization: the atrial pacing spikes are omitted

In V3, the ST elevation has increased by about 1.5 mm to almost 2 mm. 

In lead I, about 1.5 mm of ST elevation has developed.

The two leads are compared below:

There is now increased STE in both lead V3 and lead I

Let’s look at the entire picture:

Our elderly patient presented with very slight chest pain and his EKG looked normal. His pain suddenly became much worse in the ED and he became acutely diaphoretic, dizzy, and hypotensive. His EKG with worse pain now shows enough ST elevation to meet STEMI criteria. 

Surely, he should be given heparin and taken for an emergent angiogram, right?

We should take a closer look at the second EKG: 

--All leads with ST elevation have very concave ST-T complexes, with flat ST segments. 

--The ST elevation is diffuse. 

-- Leads III and V1 are isoelectric, but all other leads have some ST elevation.  In other words, STE in lead II is greater than STE in lead III. 

While the ST elevation may be deceiving, this EKG does not look like acute OMI.

The undergraduate continues:

This new EKG pattern is more suggestive of acute pericarditis.

Usually with pericarditis, some degree of PR segment depression is expected. This EKG seems to lack it.  This is becaue the rhythm is NOT sinus; it is paced.

The atrial lead of the patient’s newly implanted pacemaker has taken over the rhythm, as his native sinus rate has dropped below 60 BPM. Although no pacer spikes can be seen in this digitized EKG, the P wave morphology has changed. Pacer spikes were also visible on the paper copy. Just as with ventricular pacing, atrial pacing distorts atrial repolarization, and PR segment depression happens because of an exaggerated atrial repolarization (Ta) wave.

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Smith comments:

--If it were inferior OMI, lead III should have more STE than lead II, and there should be STD in aVL

--If it were high lateral OMI, or proximal LAD OMI, there should not be STE in lead II

In other words, the ST vector is towards leads II and V5 (towards the apex of the heart).  This is typical of pericarditis.  

But, as I always say, you diagnose pericarditis at your peril.  When the ECG suggests pericarditis, you don't just avoid activating the cath lab. Instead, you need to do more investigation to ascertain whether the patient is having OMI or pericarditis.

____________ 

The EKG was read by the conventional computer algorithm as diagnostic of “ACUTE MI/STEMI”. 

The Queen of Hearts recognizes the false positive and sees no OMI with high confidence:

Click here to sign up for Queen of Hearts Access

The emergency provider agreed with the conventional computer algorithm and thought the Queen was missing OMI; he went ahead and activated the cath lab for the STEMI protocol. The patient started receiving medications for “STEMI” (including heparin!!!) when the ED provider took a bedside echo:

This echo shows a pericardial effusion with RV invagination and bowing of the septum into the LV.  There is pericardial tamponade.

 

The ED provider canceled the STEMI protocol and updated the cath lab on the finding. 

The patient was taken emergently to the cath lab for a pericardiocentesis instead of a coronary angiogram. In the cath lab, 150 CCs of bloody fluid were drained from the pericardium. The patient’s blood pressure and symptoms improved immediately after the fluid was drained.

The post pericardiocentesis impression and plan read:

1. Pericardial effusion / tamponade - hemorrhagic, fairly acute as hemodynamically significant w only 150cc. Possible pacemaker lead perforation after after golf swing yesterday

2. Morphologic cardiac CT to eval lead perforation

3. PM interrogation eval lead thresholds

At 1451, the second troponin T came back at 24 ng/L, ruling out acute MI.

Final comment by the undergraduate: Let me know what you think! Maybe you can comment more about potential dangers for giving anticoagulants in acute pericarditis. I don't know much about that, but it seems to me that giving heparin to a patient with acute hemopericardium would be extremely dangerous. Recognition of the EKG could have avoided that. Luckily, the patient did well. 

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MY Comment, by KEN GRAUER, MD (6/18/2024):

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Today's case is humbling — fascinating — and emphasizes a number of KEY clinical concepts, most important of which is, "Always be ready to 'Think OUT of the box' when pieces of the clinical puzzle don't all add up". As a result of astute clinical reasoning and time-efficient evaluation — life-saving pericardial drainage was implemented instead of life-threatening anticoagulation.

Regular readers of Dr. Smith's ECG Blog are well familiar with what is perhaps my favorite Stephen Smith Adage = "You diagnose acute pericarditis at your peril!"

• Statistically, among patients presenting for emergency care with new chest pain — the overwhelming majority of ECGs that are diagnosed as "acute pericarditis" will turn out not to be the result of acute pericarditis. Instead, the much more common final diagnosis of such patients will be acute OMI.
• But, even 95-98% likelihood is not 100% — and on occasion pericarditis with pericardial effusion will occur, as in today's case. Dr. Smith details why the ST-T wave changes in today's 2nd tracing were atypical enough for acute OMI, that consideration of "something else" other than acute OMI was prompted. STAT Echo and minimal troponin elevation then confirmed the diagnosis.
• We review many cases of the mistaken diagnosis of pericarditis on Dr. Smith's ECG Blog (See My Comments in the June 11, 2022 post — the June 8, 2022 post — and the December 13, 2019 post, among many other examples throughout Dr. Smith's Blog).

Smith: Ken wrote this BEFORE we were provided with the original ECG #2, which clearly shows pacer spikes.

I'd add the following points to today's discussion: 

• Pacemaker spikes are not seen on the 2 tracing shown in today's case. That said — we might not expect pacemaker spikes to show because: i) This ECG is a digitized tracing, and on occasion — details such as pacing spikes are not always reliably reproduced with digitalization if they were of small size on the original ECG; — and, ii) Filter settings are not shown on these digitized tracings (I pose the question as to whether the patient has a pacemaker? — in My Comment in the January 13, 2024 post in Dr. Smith's ECG Blog — in which I review the importance of considering filter settings when assessing if the rhythm in a given ECG is or is not paced?).
• 
  
• The question arises in today's 2nd ECG as to whether the presence or absence of PR depression rules in or out acute pericarditis. As a result of decades of my admittedly anecdotal observation regarding this question — my conclusion is NO. I have seen PR depression in several leads (with PR elevation in lead aVR) in both normal individuals and in patients with acute MI — and I have seen acute pericarditis without any PR depression at all. 
• MY Approach: I continue to look for PR depression in several leads (in association with PR elevation in lead aVR) — whenever I consider the diagnosis of acute pericarditis. When I see PR depression — I consider this a minor supportive factor of the diagnosis. But when I do not see any PR depression — I realize that this in no way rules out acute pericarditis.
• And then I remember that, "Most of the time the patient in front of us will not turn out to have pericarditis" — albeit exceptions do occur, as in today's case.

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P.S. — As per Dr. Smith, I did not see the original version of the 2nd ECG at the time that I wrote my comment. I only saw the digitized tracing. As I now am provided with this original version — I’ll add the following observations:

• The pacing spikes are obvious on the original ECG — but pacing spikes are totally absent on the digitized version. This highlights the point that as helpful as ECG digitalization has become for improving our visualization — the technique is not perfect. As a result — I always spend an extra brief moment comparing the digitized version to the original tracing to ensure all essential information is reliably transmitted.
• If you look carefully in the lower lefthand corner of the original version of the 2nd ECG – you will see, “150 Hz”. This is an optimal filter setting for viewing special deflections such as pacemaker spikes — and is the reason we can see these spikes so clearly on the original ECG.