Saturday, July 16, 2022

A Middle Aged Male diagnosed with Gastroesophageal Reflux

This middle aged male with h/o GERD but also h/o stents presented to the ED with chest pain.  He had been at a clinic that day where he had complained of worsening GERD.  An EKG was recorded and interpreted as normal by the computer, the clinician, and by the overreading cardiologist.

He had an ECG recorded in triage (I am not certain whether the patient had active pain at this time; I believe he did not):

What do you think?


Here is the patient's ECG from several hours ago (which was essentially the same):
This shows minimal inferior ST Elevation that is however all but diagnostic of inferior ischemia. There is the obligatory ST depression in aVL (very subtle but diagnostic).  

There is also ST depression in V3 and V4.  We have shown conclusively that when there is such ST depression it is due to OMI of the posterior wall.  

If you put the inferior and posterior findings together, it is diagnostic of OMI

This was read as "inferior ischemia" without any other information by Dr. Richard Gray and as probable reperfused inferior-posterior OMI much later by both me and Pendell Meyers, also without any clinical information.

The computer called "Sinus Bradycardia" only (implying that everything else is normal.

The overreading Cardiologist called it only "Sinus Bradycardia" with no other findings.



Here is the old ECG from 6 years prior:
Notice the inferior T-waves have normal size here.
It is quite different, but it has been a long time.

The patient was triaged rapidly but no action was taken other than to measure troponins.  It was extremely busy in the ED and things did not get done quickly.  

The initial troponin I returned at 1500 ng/L and another ECG was recorded as the patient complained of 9/10 chest pain:
Now the T-wave in III is fully upright, suggesting re-occlusion.  
There is zero ST Elevation. 

A 2nd troponin returned at 2277 ng/mL.   

This, by itself, does not indicate persistent occlusion!  Only the symptoms and the EKG can tell you what is going on at this moment. Troponin tells you what was going on a few hours ago.

The patient was treated with aspirin, heparin, and IV nitroglycerine, and his pain persisted.  Therefore one must assume that there is persistent occlusion, and this is an indication for emergent cath lab activation by BOTH ACC/AHA guidelines and by ESC guidelines.

Therefore he was taken for emergent angiogram in the middle of the night.

A 3rd troponin returned before the angiogram was done and was 2956 ng/L

Here is the angiogram description:

The distal RCA has mild diffuse disease and bifurcates to give a large RPDA which is without 
significant stenosis. The RPAV has flush occlusion with TIMI-0 flow and is likely the culprit. 
In other words, it was a 100% occlusion of a branch of the distal RCA (TIMI-0 flow).


Peak troponin was at 8 hours after PCI and was 35,793 ng/L.  This is a large OMI that has Zero ST Elevation but can be diagnosed by ECG features other than ST Elevation!! 

Here is the post PCI EKG:


And a few hours after that:


The post PCI echocardiogram showed:

Normal estimated left ventricular ejection fraction, 57%.
Regional wall motion abnormality-mid to basal inferior wall.
Regional wall motion abnormality-mid to basal inferolateral wall.

A large infarction that does not have any ST elevation, not even subtle.



Notice the RPAV.  I'm not certain what the abbreviation is for, but I believe it is "Ramus Posterior AtrioVentricularis".  
Some interventionalists call it "The AV Groove Segment."

This illustration comes from Charles Bruen's great blog, Resus Review
Charles is another illustrious graduate of the Hennepin EM Residency; actually, the EM/IM combined residency.  Plus he did a 2 year combined EM Cardiology and Critical Care Fellowship.


Learning points:

1) There is no possible way to distinguish GERD from acute MI without BOTH EKG and troponin.

2)  A large acute OMI can be present without ANY ST Elevation

3) Occlusion of a small artery can result in a very large infarction





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MY Comment, by KEN GRAUER, MD (7/16/2022):

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

Today's case presentation by Dr. Smith highlights a number of important but all-too-easily-overlooked points. Among others, these include: i) The difficulty distinguishing between GERD vs acute MI by history (without the benefit of ECGs and troponin); andii) How a large acute OMI can occur without necessarily producing ST elevation.

I focus my attention on the initial ECG in today's case. For clarity — I've reproduced and labeled this initial tracing in Figure-1.

Figure-1: I've labeled the initial ECG in today's case (See text).



The Initial ECG: Diagnostic Until Proven Otherwise
Awareness of Dr. Smith's 1st Learning Point in today's case immediately places this middle-aged man who has known coronary disease into a "high-prevalence" group for an acute event. 
  • As per Dr. Smith — For a patient who presents to the ED with "chest pain" — it's virtually impossible to distinguish between GERD vs an acute MI without use of ECGs and troponin.
  • In a "high-prevalence" group, even before looking at the ECG — a presenting complaint of new chest pain (as was the case in today's patient) — places the onus on the treating clinicians to "rule out" rather than rule in acute disease. As a result — one's "index of suspicion" for acute ECG change has to be heightened until you can confidently prove otherwise.

Unfortunately, this was not done. The Cardiologist reviewing the initial ECG failed to appreciate diagnostic features of this initial tracing. These features are subtle — but they are definitely present and important to recognize.
  • The rhythm in Figure-1 is sinus bradycardia and arrhythmia.
  • Although there is no ST elevation in ECG #1 — there is definite ST segment coving in lead III, with subtle indication of terminal T wave negativity (curved BLUE line in this lead).
  • As I've emphasized multiple times in Dr. Smith's ECG Blog — recognition of acute posterior MI can be greatly facilitated by application of the "Mirror" Test (Please see My Comment at the bottom of the page in the September 21, 2020 post in Dr. Smith's ECG Blog). The shape of the ST-T wave in leads V2V3 and V4 is consistent with a positive Mirror Test.

  • For clarity — I've added BLUE lines over the ST segments in no less than 7/12 leads in ECG #1 that clearly show abnormal ST segment straightening — with angulation at the point that the flattened ST segment joins the beginning of the T wave upslope. Subtle-but-real ST depression is suggested in the 5 chest leads that I've labeled.
  • Finally — the T waves in leads V2 and V3 look taller-than-they-should-be given R wave amplitude in these respective leads. By the "Mirror" Test — increased anterior T wave amplitude carries similar clinical implications as the beginning T wave inversion I highlighted earlier in lead III = It is suggestive of spontaneous reperfusion.

Putting It All Together:
Today's patient was high-risk. This middle-aged male with known coronary disease presented with new chest pain. Our "threshold" has to be lowered that suspicious ECG findings are more likely to represent an acute event.  
  • While ECG abnormalities in the initial tracing were subtle — ST-T wave abnormalities were present in no less than 8/12 leads (highlighted by BLUE lines in Figure-1).
  • The positive Mirror Test with subtle-but-real ST depression in anterior leads — with hypervoluminous upright T waves in leads V2,V3 + beginning T wave inversion in lead III should suggest recent coronary occlusion, now with reperfusion until proven otherwise.

  • The markedly elevated initial troponin removed all doubt ...


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