Rhythm Nation October 2014 ANSWER!

From the hand of Dr. Yonatan Yohannes… .

This case puts the providers in a bit of a dilemma. The ECG is concerning for possible left main coronary artery (LMCA) or proximal left anterior descending (LAD) artery occlusion. However, the history and physical exam appears to be a classic presentation for pulmonary embolism (PE), not to mention that the patient also just got off of two consecutive 9-hour bus rides with 1 day in between. Therefore, the question at hand is whether the next step in this patient’s management is obtaining a CTA to confirm PE or call a Code H and send him to cath lab?

The most concerning finding on the ECG is the ST-elevation of lead aVR and V1, with ST-depressions in I, II, V5-V6. Per 2013 STEMI Guidelines, multilead ST-depression with coexistent ST-elevation in aVR may be suggestive of LMCA or proximal LAD occlusion. An occlusion of either vessel should produce ST-elevations in both aVR and V1, however the elevation in aVR should be great than V1 if the LMCA is involved. The ST-elevation of aVR in this scenario is due to infarction of the basal ventricular septum, perfused by a proximal branch of the LAD.

ECG criteria for LMCA occlusion consists of:

– Widespread horizontal ST-depression, most prominent in leads I, II, and V4-V6

– ST-elevation in aVR >1mm

– ST-elevation in aVR>V1

The differential for the ECG also includes diffuse subendocardial ischemia. This can be secondary to O₂ supply-demand mismatch in someone with no known cardiac disease or coronary insufficiency due to severe 3-vessel disease (>50% occlusion of each). Since aVR is electrically opposite of leads aVL, I, and V4-V6, ST-depressions in these leads can cause a reciprocal ST-elevation in aVR (as opposed to an ST-elevation in aVR due to infarction of the basal septum). Some physicians would argue that ST-elevations in aVR are more likely to be from non-ACS causes (i.e. diffuse subendocardial ischemia) than traditional STEMIs⁴, therefore it is reasonable to manage medically while searching for a cause, in discussion with cardiology of course, as opposed to reflexively activating the cath lab.

Based on this patient’s H&P it appears that PE should be at the top of our differential. However, the ECG (which we often see before actually seeing the patient) is concerning for possible cardiac pathology. How should we proceed when our history and physical screams one diagnosis, but the ECG says another?

This case is an example of ST elevations that you see in leads I and aVR may reflect right-sided strain and that TW inversions in inferior leads II, III, aVF may be signs of massive PE instead of STEMI.

Case summary:

The ED did not activate the cath lab initially. Cardiology was consulted and the patient was loaded on heparin and plavix, then taken to the cath lab based on the elevated troponin and anterior wall motion abnormality on the fellow’s bedside echo. Cath summary showed “all coronary arteries WNLs” and noted a grossly diminished cardiac output. Immediately afterwards, the patient was started on a heparin drip and his D-dimer, sent from the ED, was now back at approx 25,000 (remember, normal should be < 500). The patient received a VQ-scan overnight confirming diffuse segmental PEs. An echo the following day found a “moderate size, highly mobile mass in the right atrium” likely a thrombus which explains the diffuse segmental PEs. The patient was put on a heparin drip in the hospital and then sent home on coumadin.

References

O’Gara, P. T., Kushner, F. G., Ascheim, D. D., Casey, D. E., Chung, M. K., De Lemos, J. A., . . . Zhao, D. X. (2013). ACCF/AHA Guidelines for the Management of ST-Elevation Myocardial Infarction. Circulation, 127, e362-e425.
Martindale, J. L. & Brown, D. F. M. (2012). Rapid Interpretation of ECGs in Emergency Medicine: A Visual Guide. Philadelphia, PA: Lippincott Williams & Wilkins.
Burns, E. (2014). ST Elevation in aVR – LMCA Occlusion. Life in the Fast Lane. Retrieved from http://lifeinthefastlane.com/ecg-library/lmca/.
Smith, S. (2013). Middle Aged Woman With Asystolic Cardiac Arrest, Resuscitated: Cath Lab? Smith’s ECG blog. Retrieved from http://hqmeded-ecg.blogspot.com/2013/10/middle-aged-woman-with-asystolic.html.

Supervised by Dr. Jennifer Martindale.

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2 Comments

Nathan · October 26, 2014 at 11:36 am

This pattern also seems to be relatively common in post cardiac arrest patients who have intracranial bleeds. About 50% of ROSC patients have acute coronary occlusion and will benefit from PCI (regardless of ecg findings) but for the 15% with SAH a diffuse ischemia pattern is often seen. Mortality from SAH with cardiac arrest is virtually 100% so you should at least consider this diagnosis if you see diffuse ischemia after a cardiac arrest.

Ian deSouza · October 30, 2014 at 8:01 am

Great job, Yohannes. This is a nice case demonstrating that “loading the [proverbial] boat” (especially with unsupervised consulting residents) without taking a comprehensive approach to a critical patient, can lead case management astray. The EPs here should be commended for their attention to the HPI and low pre-test probability of MI rather than simply focusing on the ECG’s ST-elevations. It would have nice if RV was examined with the bedside US – again WE should be doing this, cardiology residents are suspect in their abilities to do so – but RV strain and thrombus may have also been diagnosed more rapidly with ventriculography during the angiogram. This could have allowed for more definitive, focused treatment of thrombolysis for moderate PE.