Tuesday, July 7, 2020

An Very Elderly Male with Epigastric pain, "ischemic ECG" and Interesting Imaging.

A very elderly male presented with epigastric pain on and off for 36 hours.

His exam was unremarkable.

Here is his ED ECG:
There appears to be atrial fibrillation (no previous history).
Extreme Left Axis Deviation
There are inferior and anterior QS-waves suggestive of previous MI
There is inferior ST Elevation, with reciprocal ST depression in aVL, as well as in V1, suggestive of inferior and right ventricular MI
There is ST depression maximal in V2 and extending to V6.
What do you think?














Myocardial infarction was suspected.

An initial troponin returned at 0.058 ng/mL (URL = 0.030 ng/mL)

A chest X-ray was obtained:
This shows the stomach in the chest



A CT was obtained (here is a sagittal view):

This shows the stomach behind the heart and compressing the heart against the anterior chest wall.
Here are a couple coronal sections:

This is a section anterior to the posterior herniated stomach

Here is a section behind the heart showing the herniated stomach
This section is behind the heart, showing the very large, distended stomach




Clinical course:

A nasogastric tube was placed and the stomach emptied.

Another ECG was recorded:
There is now sinus tachycardia and all ST changes suggestive of ischemia are resolved.


Troponin peaked at 0.078 ng/mL and then decreased to undetectable.

Cardiac echo showed no wall motion abnormality.

Learning Point:

Anatomic pathology can alter the ECG.  In this case, the compressed heart resulted in an ischemic appearing ECG.



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MY Comment by KEN GRAUER, MD (7/7/2020):
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Today’s case serves as a welcome reminder that non-cardiac structural conditions may alter the ECG — sometimes in dramatic fashion! This case features an elderly patient who presented to the ED with a large hiatal hernia, in which the gas-filled stomach protruded well into the chest cavity. As shown on CT in Dr. Smith’s discussion (above) — marked gastric distention with anatomic position directly behind the heart resulted in cardiac compression against the anterior chest wall.
  • NOTE: HH (Hiatal Hernia) is not necessarily a benign condition. The patient in today’s case presented with a 36-hour history of epigastric pain severe enough to prompt a visit to the ED.
  • Additional symptoms reported with a large hiatal hernia (in which a significant portion of the stomach has entered the thoracic cavity) include — dyspnea (especially with activity) — difficulty feeding — and, precipitation of cardiac arrhythmias.
  • The mechanism for producing arrhythmias is thought to result from cardiac compression — which could be of the LA (Left Atrium), causing atrial arrhythmias (especially AFib)  and/or of the mitral annular region, including the adjacent basal inferior LV (Left Ventricular) wall. Autonomic influence may contribute to arrhythmogenesis by compression (therefore stimulation) of the vagal and sympathetic nerves. Gnanenthiran et al. postulated that one or both of these mechanisms may have been the cause in their Case Study Report of Ventricular Tachycardia that was felt to be caused by HH-induced cardiac compression (Heart Rhythm Case Reports 4:362-366, 2018).
  • In addition to arrhythmogenesis — large HH may also produce a variety of ECG abnormalities, including ST segment depression and/or elevation  T wave inversion in multiple leads — and/or alteration in QRS morphology.

“Take-Home” PEARLS from Today’s Case:
As per the Learning Point by Dr. Smith — Anatomic pathology can alter the ECG. Other potential examples of non-cardiac, chest cavity structural conditions that may result in significant ECG alterations include: ipneumothorax; ii) pleural effusion; iii) space-occupying lesions (including benign and malignant tumors); ivchest wall deformities; v) large body habitus; andvi) anatomic variants (including dextrocardia and the various types of situs inversus). Other than the well described conditions of pericardial effusion and the various types of situs inversus — I found literature on this subject was limited. Nevertheless, brief perusal of the literature I did find left me with the following impressions:
  • Each of the above conditions may be associated with ECG abnormalities similar to those I listed above for large HH = ST depression and/or elevation — T wave inversion — axis shift — poor R wave progression — Q waves and/or QS complexes. As a result — each of the above conditions is prone to producing a pseudo-infarct pattern, as occurred in today’s case.
  • Therefore — Don’t Forget to order (and look at) the patient’s Chest X-Ray. IF your patient’s primary symptom is chest discomfort — and, the ECG shows worrisome ST-T wave abnormalities — it is all too EASY to rush down the path toward acute cath lab activation, only to later discover some anatomic abnormality that was obvious on a simple chest X-ray.

Taking Another Look at the ECGs in Today’s Case:
For clarity — I’ve put both of the tracings from today’s case together in Figure-1. Consider the following questions:
  • HOW did YOU interpret ECG #1?
  • ECG #2 was obtained after nasogastric tube insertion that decompressed the stomach. Has this patient had prior infarction(s)?

Figure-1: The 2 ECGs in today’s case (See text).



MY Thoughts on ECG #1:
There is significant baseline artifact, with intermittently spaced small vertical spikes. These are not pacemaker spikes.
  • The overall rhythm is irregularly irregular. P waves are absent. Therefore — the rhythm is AFib, here with a controlled ventricular response.
  • The QRS complex appears to be minimally widened (between 0.10-0.11 second in duration). QRS morphology looks supraventricular.
  • There are deep QS complexes in each of the inferior leads. There appears to be a tiny, initial positive deflection in leads V1 and V2. Thereafter — QRS complexes vary between showing either a similar, small initial r wave vs a QS complex. The R wave in the chest leads never exceeds 2 mm in amplitude, such that transition never occurs.
  • As per Dr. Smith — there is slight-but-real ST elevation in each of the inferior leads (albeit with an upward-concavity ST segment shape) — with reciprocal ST depression in both high lateral leads (leads I, aVL).
  • In the chest leads — the ST elevation in lead V1 is clearly abnormal. The remaining chest leads all show ST depression, which (as per Dr. Smith) is most marked in lead V2. This chest lead J-point ST depression rises to disproportionately elevated and peaked T waves in leads V2-thru-V6.

My IMPRESSION: In a patient with new symptoms — ECG #1 is certainly consistent with ACS (Acute Coronary Syndrome) — and could reflect acute infarction in progress.
  • Additional Thoughts on ECG #1 — The slight QRS widening without manifestation of any specific conduction defect + the AFib rhythm suggest that this patient is likely to have some form of underlying heart disease. The deep QS complexes in each of the inferior leads — and remarkable lack of any R wave progression in the chest leads looks bizarre. Clearly this overall picture could reflect prior extensive infarction — though I was struck by the unusual and similar likeness of the QRS-ST/T wave appearance in leads V2-thru-V5. I would have LOVED to find a prior ECG on this patient to help sort out what was “new” vs “old” (vs “new + old” — although in the absence of any prior tracing, the above-described ST-T wave changes mandate assuming ACS until proven otherwise.

What Happened After NG Tube Decompression:
I found it especially interesting to compare lead-by-lead the appearance of ECG #2 with initial ECG #1:
  • As per Dr. Smith — AFib is no longer present in ECG #2. Resumption of sinus rhythm (sinus tachycardia at ~105/minute) is challenging to appreciate because: i) there is even more baseline artifact in ECG #2 compared to what was seen in ECG #1 (especially in leads II and V1, which typically are the best leads for spotting sinus P waves); ii) P wave amplitude is small; andiii) P wave morphology varies from one beat to the next. That said — Return to regularity of the rhythm and the RED arrows highlighting atrial activity in ECG #2 are consistent enough to confirm resumption of sinus rhythm after NG decompression.
  • Deep QS complexes remain in each of the 3 inferior leads.
  • Although there is slight increase in R wave amplitude in lateral chest leads V5 and V6 — R wave progression remains extremely poor in ECG #2.
  • Interestingly — there is some beat-to-beat variation in R wave and S wave amplitude in the chest leads of ECG #2. This is probably the resut of respiratory variation from movement of the diaphragm (which is contiguous to the portion of the stomach protruding into the chest cavity, and lying adjacent to the posterior surface of the heart).
  • The “good news” (as per Dr. Smith) — is that the acute-looking ST-T wave changes in leads V2-thru-V5 of ECG #2 have greatly improved. I’m not convinced that ST elevation in the inferior leads is less — but there clearly is less J-point ST depression in high lateral leads I and aVL — and the abnormal ST elevation in lead V1 has probably resolved (though this is hard to assess given all the artifact in V1).

My CONCLUSION: Prior to reviewing the literature for discussing this case — I had not fully appreciated the impact of the mechanism of cardiac compression as a causative factor in: i) altering QRS morphology; iiprecipitating supraventricular and/or ventricular arrhythmias (including VT, which can be sustained) — andiiiproducing ST-T wave changes (ST elevation and/or depression) that may mimic old or new infarction.

  • CT imaging (as shown by Dr. Smith) clearly suggests there was compression of cardiac structures in this case by the distended portion of the stomach protruding into the chest cavity. Presumably, the degree of cardiac compression was greatly reduced following NG decompression — which corresponded to resolution of AFib and marked reduction in acute-looking ST-T wave changes in ECG #2.
  • That said — this patient still has a large hiatal hernia (most likely with a large portion of the stomach still protruding into the thoracic cavity) — even though the component of ischemic- and arrhythmia-inducing cardiac compression appears to be relieved.
  • HOW MUCH of the inferior and anterior lead QS complexes might be a result of this patient’s large, protruding hiatal hernia? Was an ECG ever done before development of the hiatal hernia? I’d LOVE to know IF the unusual inferior QS complexes and persistently poor R wave progression would resolve if this patient’s large hiatal hernia was surgically corrected. Finally — Did this patient have prior infarction(s)? Unfortunately — I don’t think we can answer this question with only the information we have at hand ...
  • Clinically — the decision as to whether or not this elderly patient should undergo surgical correction of his large hiatal hernia may prove more difficult than I would have thought prior to researching this topic. Balancing this patient’s advanced age and underlying comorbidities — is convincing CT scan evidence of direct cardiac compression by the hiatal hernia + ECG evidence that recurrent gastric distension risks AFib recurrence with significant cardiac ischemia.
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  • TO OUR READERS: Do YOU have cases of non-cardiac chest cavity structural abnormalities producing remarkable ECG changes that you’d like to share? If so — please SEND them to us at the CONTACT LINK for Interesting ECGs (in the righthand column of this blog, near the top of the page).
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10 comments:

  1. Hey Steve!
    Interesting case and a pretty good Acute Proximal RCA Occlusion mimic. What catches the eye first is the Precordial depression mimicking Posterior MI. Next the ST elevation in V1 suggestive of RV MI. Then to the Inferior Leads ST Elevation and finally to aVL and I for reciprocal change. It's all there and a pretty good mimic but what made me doubt the diagnosis is the Inferior T waves just don't have the size nor seem to have the "look".
    Sam

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    1. Thanks Sam — Good to hear from you! You, myself & Steve are all on the same line of the same page! In addition to the points you make — to me, the similar shape of the QRST complexes (especially in leads V3-thru-V6) was very peculiar — which together with those slightly widened inferior lead QRS complexes (without there being a recognizable BBB) did not (as you say) seem to have "the look". THANKS again for your comment! — :)

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  2. The bizarre frontal axis pushed me away from AMI; and I too would love to see a pre-HH ECG and a post-decompression ECG. Fascinating!

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  3. Thanks for your comment, Christopher. Haven't heard from you in a long time!

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  4. Very interesting case, thank you very much.
    the STD and peaked T waves arising form the depressed ST Segment reminds me of de Winters sign, which has been associated with LAD occlusion especially when there is also STE in avR. (There is slight STE in avR?). Ist also called a STEMI equivalent.
    i for myself at the bedside of this Patient would be concerned to guess how much of the ischemic changes in the ecg are due to compression and how much is possibly an OMI at the same time, that has to go immediatly to the cath. lab. To do the X Ray (or CT scan)and to place a nasogastric tube to decompress and then make an ecg again is time consuming if there is possibly an ongoing OMI.
    Thank you for your comment


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    1. THANK YOU so much Christian for your comment! Although there IS some resemblance between ECG #1 and de Winter T waves — an important difference is that in ECG #1 from this case, the LENGTH (duration) of the depressed ST segment in multiple chest leads is much LONGER than the usual J-point ST depression that RAPIDLY rises to an overly large (hyperacute) T wave with de Winter T waves. I refer you to My Comment in the May 2, 2019 post of Dr. Smith’s blog = http://hqmeded-ecg.blogspot.com/2019/05/doctor-should-we-activate-hospitals.html — in which I discuss ECG findings, including a figure showing several variations in chest lead T wave appearance, taken from the original NEJM Letter by de Winter et al. I think you’ll agree that those T waves differ from the longer-duration flat portion of the ST segment in ECG #1 of today’s case.

      Otherwise — I’d address the 2nd part of your comment by first saying, “Ya gotta be there!” — since it is often difficult to know exactly what one would do based on reading the “written word”. That said — there are several features in this case suggesting that there WAS time to get the chest X-ray. These include: i) the history (ie, not new-onset worrisome chest pain — but rather 36 hours of “on-off” epigastric pain); ii) a lack of “stemi-like” ST elevation (ie, minimal upward-sloping inferior lead ST elevation — and anterior lead ST elevation limited to lead V1); and iii) the overall “Gestalt picture” of ECG #1, that to me looked somewhat “off” from an acute STEMI (that I describe above in My Impression). iv) Finally — there is the potential DOWNSIDE of rushing this patient off to the Cath Lab IF indeed ischemic changes were the result of cardiac compression induced by direct pressure from gastric distension (since doing stat cath on this patient would have DELAYED the real treatment in this case, which is NG tube decompression — keeping in mind that case study I cite above of sustained VT induced by HH-induced cardiac compression severe enough to produce ECG changes).

      I’d add that one need NOT wait for a CT scan in this patient! Instead — a simple chest X-ray (such as the one shown above in this case) should be more than sufficient to suggest cardiac compression from gastric overdistension as the probable cause of this patient’s symptoms and ECG findings. Again, this is NOT a simple decision-making process — and one HAS to “be there” to know for sure how this would play out — but if expedited, it shouldn’t take more than minutes to get a stat chest x-ray (which should be enough to make the diagnosis in this case). GREAT discussion with important learning points!

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  5. Thank you for your comment and explanation, i appreciate this very much, your blog has become a very valuable resource of continuing learning and education for me.

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