An elderly woman transferred to you for chest pain, shortness of breath, and positive troponin - does she need the cath lab now?

Written by Alex Bracey, with edits by Smith and Meyers

A female in her 70s presented to the ED at sign out while working in our acute zone (medium acuity). I picked up the chart and the triage note indicated that the patient was transferred from another hospital, with "EKG changes"and elevated troponin, for cardiology evaluation of NSTEMI. Symptoms were ongoing.

Interest now piqued, I looked at the EKG and saw the following:

What do you think? Baseline for comparison below.

This is nearly pathognomonic! 

Of what?

Baseline on file from outside hospital:

This is her first ECG at our hospital:

Meyers ECG interpretation: The new ECGs show sinus tachycardia with convex ST segments leading into large T-wave inversions in the anterior and inferior leads. The morphology is consistent with many prior examples of acute right heart strain we have shown on this blog. Also, even if these T-wave inversions had been due to reperfusion of OMI (despite the fact that they are not the right morphology for this), they would usually coincide with significant improvement in the patients symptoms, whereas this patient has ongoing severe shortness of breath during this ECG. The T-wave inversions are also not "too big" for the QRS, meaning out of proportion for reperfusion or acute right heart strain, such as those due to takotsubo cardiomyopathy as seen in this post.


Back to the case:

Having recently seen a post on pulmonary embolism (this one), I was immediately concerned that the patient had an acute PE, even without seeing the patient. 

I took the ultrasound with me into the room and found an older woman on nasal cannula, breathing heavily and rapidly, but alert and able to tell me in between gasping breaths that she had become suddenly short of breath the day before presentation. She was normotensive, but profoundly hypoxemic when off of nasal cannula support. While obtaining the history I was able to get these images on bedside ultrasound:

TAPSE = Tricuspid Annular Plane Systolic Excursion, a measure of how far the tricuspid annular plane moves during systole, which is reduced in right heart strain of any cause, chronic or acute. Less than 18 mm is considered reduced, here is it is measured at 0.89 cm.

Here is the apical 4 chamber view:



The right ventricle is on the left side of the screen. The RV is dilated and does not appear to decrease in size during systole. There is also McConnell's sign (relative hyperkinesis of the RV apex relative to the RV free wall in the setting of RV strain). There is also paradoxical motion of the septum, with bowing into the LV.


Here is the parasternal short axis view:



The RV is at the top of the screen (closest to the probe). The RV is much larger than the LV, and you can see the "D sign", where the interventricular septum is flattened by high RV pressure into the straight portion of the capital letter "D."

With this constellation of symptoms, I was very confident that the patient had an acute, significant PE causing heart strain. We started a heparin drip. The patient continued by stating that she had injured her back 3 months ago and had barely moved from the couch in the subsequent months. This shortness of breath coincided with her attempting to be more mobile yesterday.

CT pulmonary angiogram demonstrated the following:

This shows very large bilateral main pulmonary artery filling defects consistent with PE.

The patient was transferred to the critical care ED where, after discussion with pulm/cc the patient received half dose tPA. Over the next 12 hours she had a profound improvement in her work of breathing and did not require supplemental oxygen by her discharge 4 days later. She was discharged to home on a DOAC and with home physical therapy. 

Learning Points:

The ECG can be diagnostic of severe acute right heart strain. You must be able to recognize this pattern and distinguish it from the findings of Occlusion MI. 

See this post for more examples of the characteristic morphology of acute right heart strain.

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Comment by KEN GRAUER, MD (4/5/2019):

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Our THANKS to Dr. Alex Bracey for this instructive presentation with excellent discussion regarding an older woman who was transferred to the ED from an outlying hospital for complaints of chest pain, shortness of breath, and a positive initial troponin level.

• I focus my comments on: i) Some general concepts regarding use of the ECG as part of the clinical diagnosis of Acute PE: and, ii) Some interesting aspects about the initial ED ECG in this case ( = ECG #1, which I’ve reproduced and labeled in Figure-1).

Figure-1: The initial ED ECG in this case ( = ECG #1) — obtained from an older woman with shortness of breath, chest pain and a positive troponin (See text).

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COMMENTs Regarding ED Diagnosis of Acute PE: Perhaps the most important point to “Take Home” from this case — is the multifaceted way that definitive diagnosis of acute PE can so rapidly be made in the ED.

• I have to acknowledge that I did not get a sense of the true “essence” of the history in this case from the 2-line title of this post. I say this not as a negative (since I would have chosen a nearly identical initial description for this case in the interest of optimizing teaching points). My point is merely to emphasize that, “Ya gotta be there!” when assessing each new patient assigned to you. Dr. Bracey realized within seconds on entering this patient’s room — that the true history was screaming acute respiratory distress (the patient was profoundly hypoxemic, oxygen dependent and markedly dyspneic — and, she described sudden onset of her symptoms just the day before). The history of reported chest pain seemed an “afterthought”. Translation — Even without seeing the patient’s initial ECG, or before proceeding with any diagnostic assessment — this type of history and clinical presentation are saying, “I have a large acute PE until you can prove otherwise”.
• Diagnostic considerations from the ST-T wave changes seen in ECG #1 include acute/recent coronary disease, Takotsubo cardiomyopathy, and acute PE. Even before addressing the astute ECG interpretation pearls by Dr. Meyers (that strongly favor acute PE as the diagnosis) — the true history in this case (stated in the preceding bullet) greatly increases statistical likelihood that ST-T wave changes in ECG #1 are due to acute PE.
• Bedside Echo was then performed by Dr. Bracey. Given the clinical presentation — this Echo was diagnostic!
• KEY Point: Although not directly stated by Dr. Bracey — it sounds like it took no more than a very few minutes of assessment by history, the patient’s profound hypoxemia, the initial ECG + Bedside Echo to make a definitive diagnosis of Acute PE. CT pulmonary angiogram provided further confirmation — though this wasn’t needed for initiation of optimal treatment.

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Regarding the Initial ECG: I interpreted the initial ECG obtained in the ED on this patient ( = ECG #1) as follows:

• Descriptive Analysis — There is relatively low voltage. The rhythm is sinus tachycardia (RED arrows) — with atrial quadrigeminy (every-4th-beat occurs early and manifests a different P wave morphology => every 4th beat is a PAC = YELLOW arrows). The PR and QRS intervals look normal; the QTc appears at least borderline prolonged. The frontal plane axis is normal. The deep negative component to the P wave in lead V1 is consistent with LAA (Left Atrial Abnormality). No other ECG sign of chamber enlargement is seen. The most remarkable findings are dramatic ST-T wave changes in multiple leads (ST segment coving with no more than minimal ST elevation in leads III, aVR, V1; deep symmetric T wave inversion in a number of leads; reciprocal ST-T wave appearance in leads III and aVL).
• Clinical Impression — As per Dr. Meyers, ST-T wave changes and the clinical course of this patient were not as would be expected for acute coronary reperfusion (unless perhaps there was acute multi-vessel disease ... ). Instead — the anterior and inferior deep, symmetric T wave inversion in multiple leads is much more consistent with a diagnosis of acute PE.

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Additonal Points: The ECG will often not be helpful for diagnosing acute PE. That said — this case illustrates one instance in which the ECG (together with this patient’s clinical presentation) strongly suggested the diagnosis even before bedside Echo and CT pulmonary angiogram were done.

• In an adult with new-onset dyspnea or pleuritic (or atypical) chest pain — the finding of anterior T wave inversion (ie, in leads V1,V2,V3) will much more often be due to acute PE than to acute coronary disease. This is especially true IF there is also inferior T wave inversion (in leads II, III, aVF) — which is the other lead area that characteristically manifests ST-T wave changes of acute RV “strain”. These ECG findings are consistent with the pattern of T wave inversion that we see in ECG #1 (which in addition, shows a lesser degree of T wave inversion extending as far out as the lateral chest leads).
• Sensitivity of the ECG for suggesting the possibility of acute PE is better with larger (especially submassive) PEs. When ST-T wave changes of acute PE are as marked and “acute-looking”, and as extensive as they are in Figure-1 — it is almost certain you are dealing with a very large PE. In contrast — small-to-moderate size PEs are far less likely to show much more than sinus tachycardia with nonspecific ST-T wave changes.
• There are other ECG findings to look for that may suggest acute RV “strain” — especially when several of these are seen in the “right” clinical setting. These other ECG findings include right or indeterminate frontal plane axis — S1Q3T3 sign — RAA (right atrial abnormality) — complete or incomplete RBBB — prominent R wave in lead V1 — persistent deep S waves in lateral chest leads — and atrial fibrillation. Although we don’t see any of these other ECG findings (apart from sinus tachycardia) in this case — the clinical history + the marked and very characteristic ST-T wave abnormalities in Figure-1 were more than enough to strongly suggest the diagnosis of acute PE here.
• Beyond-the-Core: Did You Notice that the degree of ST-T abnormality in lead V2 is much less than in both lead V1 and lead V3? This finding was unexpected because: i) It does not make physiologic sense for normal QRST progression to manifest such large QRS amplitude in this single lead (V2) — when the T wave is so much more deeply inverted in other neighboring leads (V1, V3, V4) with much smaller QRS complexes; and, ii) Acute RV “strain” is generally maximal in anterior chest leads — so the surprisingly shallow T wave inversion we see in lead V2 does not make sense from this perspective either. I suspect there is some chest lead malposition of lead V2 — and that the “real” amount T wave inversion in lead V2 is much closer to what we see in leads V1, V3 and V4.
• Finally — Did You Notice the change in morphology for beats #1 and #4 in lead III — compared to the much smaller and multi-phasic QRS complex for beats #2 and #3 in this lead? While clearly an academic point that does not affect clinical management — I think it helpful to point out that this change in QRS morphology is not due to aberrant conduction — because if it were, then it would be the PACs that should be the complexes that look different (ie, beats #2 and #6 — and not #2 and 3). Instead — this change in QRS morphology is most probably the result of respiratory movement in this acutely dyspneic patient! PEARL: Leads III and aVF are vertically positioned (ie, viewing the heart from under the diaphragm) — and in my experience, these are the leads most prone to occasionally showing fairly marked beat-to-beat variation in QRS morphology, especially in dyspneic patients.

Our THANKS again to Dr. Alex Bracey for sharing this highly insightful case with us!

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FOR MORE:

• For more on “My Take” on the ECG diagnosis of Acute PE & RV Strain — CLICK HERE.