Texted from a former EM resident: 70 yo with syncope and hypotension, but no chest pain. Make their eyes roll!

A former resident texted me this case: 

"Hey Dr. Smith. Hope you’re doing well! How excited would you have been about this case?" 

Here is the case:

Report from EMS was witnessed syncope, his son did CPR, but the patient had pulses when EMS arrived. When the patient arrived in the ED, he was still hypotensive in 70s, slowly improving with EMS fluids. No Chest Pain, but somnolent. 

Here is the ED ECG (a photo of the paper printout)

What do you think?

Smith: There is 1mm of STE in V1 and almost 1.5mm in V2.  There are QS-waves in V1-V3 suggesting old anterior MI with persistent ST Elevation (LV aneurysm morphology), but I have written a couple papers showing that in LV aneurysm, the T-wave is not > 0.36 x the QRS amplitude in any of V1-V4.  The highest ratio here is in V4 at 1/1.5 = 0.67.   Next is V2 at 5/14.5 = 0.34.   The fact that this is syncope makes give it a far lower pretest probability than chest pain, but it was really more than syncope, as the patient actually underwent CPR and had hypotension on arrival of EMS.

1. Smith SW.  T/QRS Amplitude Best Distinguishes Acute Anterior MI from Anterior Left Ventricular Aneurysm.  American Journal of Emergency Medicine 2005; 23(3):279-287.

https://www.sciencedirect.com/science/article/abs/pii/S0735675705000811

 

2. Klein LR.  Shroff G.  Beeman W.  Smith SW.  Electrocardiographic Criteria to Differentiate Acute Anterior ST Elevation Myocardial Infarction from Left Ventricular Aneurysm.   The American Journal of Emergency Medicine 2015; 33(6):786-790.  https://www.sciencedirect.com/science/article/abs/pii/S0735675715001904

So I responded with these words:

Smith: "There are QS waves, which suggest old MI.  But the T-waves in LV aneurysm are not this big.  This is LAD Occlusion until proven otherwise."

Smith: "What did you do?"

Former resident: "I activated, ran it through the queen and she agreed but cardiology wasn’t excited."

The Queen say OMI with High Confidence.  

Explainability shows: she sees the T-waves AND the QRS in lead V2, but also in leads V3-4.

Smith: "Did they take him right away to cath?"

Former Resident: "They took him but they rolled their eyes at me (Smith editorial comment: how often have they rolled their eyes at YOU?). They said it looked similar to his old one (in my opinion, similar, but not similar enough to be able to say no OMI)."

Smith: "What was the outcome?"

Former resident: "Just saw cath report, LAD stent was 100% acutely occluded."  

They of course opened and stented it.

Former resident: "The biggest piece for me was the size of the T waves in relation to everything else. You taught us well!"

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MY Comment, by KEN GRAUER, MD (9/11/2024):

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Among the important concepts brought out by today's case are the following: 

• #1) — Is acute OMI a common cause of syncope?
• #2) — How to distinguish between LV aneurysm vs new infarction?

To emphasize (as noted by Dr. Smith) — today's patient did not present only with syncope. Instead — the "syncopal episode" prompted the patient's son to start CPR, and was associated with persistent hypotension. That said — syncope remains a common reason patients seek emergency care — so it is worth addressing how often acute MI is the cause.

• Among patients who present purely for “syncope” — our  greatest concern is focused on those with a cardiac-related etiology for their syncope — since longterm prognosis is poorest for these patients unless a “fixable” etiology is discovered.
• Acute MI per se usually does not depress cardiac function and blood pressure enough to cause syncope (Mostafa et al — J Com Hosp Intern Med Perspect 13(4):9-12, 2023-). But especially with infero-postero OMI, it may do so indirectly — by activating the BJR (Bezold-Jarisch Reflex) — which in response to sympathetic activation (and/or in association with coronary reperfusion) — may activate mechanoreceptors that are primarily located in the infero-postero wall of the LV, producing a potent parasympathetic effect that may lead to reflex bradycardia, peripheral vasodilation and hypotension (Cadogan — Life-In-The-Fast-Lane, 2022 — and — Holland, Stouffer — JSCAI 1(2),2022).
• Other cardiac-related causes for syncope associated with acute MI may include malignant ventricular arrhythmias and bradyarrhythmias including AV block.
• The "good news" — is that a cardiac-related cause of syncope is unlikely if the initial ECG is normal, and cardiac monitoring in the ED fails to reveal significant arrhythmia.

LV Aneurysm vs New Infarction?

The initial ECG in today's case was recognized as definitely abnormal — but the question arose as to whether this ECG indicated old infarction vs a new acute event.

• QOH (Queen Of Hearts) and Dr. Smith's former resident immediately diagnosed acute OMI — but providers in the ED thought the ECG findings "looked old".
• As per Dr. Smith — T/QRS amplitude measurement clearly indicated that rather than LV aneurysm, the elevated ratio suggested acute infarction until proven otherwise. 

I thought qualitative assessment of the initial ECG (that I have labeled in Figure-1) — clearly favored new on-top-of old infarction until proven otherwise:

• At the least — ECG #1 is diagnostic of previous infarction(s) at some point in time because of diffuse abnormal Q waves. Not only are such Q waves seen in all 3 inferior leads — but they are also present in all 6 chest leads (QS complexes in leads V1-thru-V4). Most of these Q waves are unusually wide with respect to QRS amplitude in the lead being looked at — as well as fragmented in multiple leads, including lead V3 (BLUE arrow) and leads III, aVF, V2 and V4.
• But in addition to prior infarction — lead V2 is clearly "off", as the ST segment straightening in this lead "looks" acute — and the disproportionate amount of ST elevation in V2 is visually beyond that expected with simple LV aneurysm.
• In the context of this hyperacute appearing ST-T wave in lead V2 — the other 2 leads within the RED rectangle support the impression of acute injury until proven otherwise (especially the ST segment straightening in lead V1, with a disproportionate amount of ST elevation for this lead).
• I would not have been convinced by the subtle ST elevation in the inferior leads alone — but I thought the ST segment coving and T wave inversion in lead aVL added support that the above highlighted findings in leads V1,V2,V3 must be assumed acute until proven otherwise.

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