Syncope, hypotension, vomiting and diaphoresis in a 60-something male with Diabetes and Hypertension

I was texted this ECG by one of my partners, with the following history: 

A 60-something male with diabetes and HTN presented with syncope. Per EMS report, the patient had a syncopal episode at work. On medics arrival, patient noted to be pale and diaphoretic, SBPs 60-80s, complaining of nausea and had one episode of emesis en route, possible hematemesis. 

There was no chest discomfort, though the patient was non-English speaking and reportedly "stoic".

What do you think?

This was my response, in quotes: 

"I have a sneaking suspicion that this is a mimic.  

Tough one!  

No STD in aVL.  

Prominent J-waves in III, aVF. 

STE II > III.  

All of those go against acute OMI."

My partner had already activated the cath lab, and the angiographer agreed, which is fine with me!

The angiogram was negative.

A formal echo showed 80% EF and no wall motion abnormality

The patient ruled out for MI by troponins

Here is the post angiogram EKG:

No change, proving that this is the baseline ECG.

Learning Points:

1. There are many ECGs that mimic OMI and they may be very difficult to differentiate from OMI.

2. It takes expertise to find the distinction.

3. Syncope without chest discomfort has a very low pretest probability

4. It is no crime to have a false positive cath lab activation.

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MY Comment, by KEN GRAUER, MD (12/10/2022):

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Sometimes an ECG raises more questions than it answers! Such is the case with today's patient — as both the initial ECG and the tracing obtained after cardiac catheterization had me literally "scratching my head".   

• The "good news" — is that the angiogram was negative — Echo showed an excellent EF = 80% (with no wall motion abnormality, no more than borderline LVH — but no RVH) — troponins were negative — and an acute cardiac problem was ruled out!
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• That said — the 2 ECGs in today's case merit discussion. For clarity — I have put both tracings together in Figure-1: 

Figure-1: Comparison of the 2 ECGs in today's case.

MY Thoughts on the ECGs in Figure-1:

Today's patient is a man in his 60s — who presented to the ED following a syncopal episode. The patient was markedly hypotensive at the time ECG #1 was recorded. My initial impression of this 1st ECG in today's case was the following:

• The rhythm is sinus at ~85/minute. Intervals (PR, QRS, QTc) are normal.
• There is marked RAD (Right Axis Deviation) — with the QRS predominantly negative in lead I.
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• Regarding Chamber Enlargement — There is no sign of atrial abnormality (P waves if anything — being normal but relatively small in size). The S wave in lead V2 is deeper-than-usual (ie, >22 mm) — but definite criteria for LVH are not met. RVH is a possibility (marked RAD; R>S in lead V1 — See below).

Regarding Q-R-S-T Changes:

• Q waves are present in each of the inferior leads. The initial deflection in lead II is negative (ie, a "Q" wave) — but the QRS in this lead is tiny and fragmented. The Q waves in leads III and aVF are relatively wide (ie, potentially indicative of infarction at some point in time).
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• R Wave Progression — is notable for the presence of an R>S wave in lead V1. After lead V1 — relative R wave amplitude progressively decreases. ECG #1 is remarkable for the presence of a surprisingly small QRS complex in lead V5 — and — a tiny QRS in lead V6!
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• ST-T waves in ECG #1 are "eye-catching"! In view of the small size of the QRS complex in leads II and aVF — there is considerable ST elevation. Other leads show a much more modest amount of ST elevation. But the most remarkable feature — is the "hyperacute-appearing" ST-T waves in multiple leads (ie, in leads I, II, aVL, aVF; and in V2-thru-V6). The T wave is flat in lead III and shallowly inverted in V1 — but there is no ST depression on this tracing. 

Putting It All Together:

I was initially shown ECG #1 without the benefit of any history. Although my obvious concern given inferior lead Q waves, ST elevation and hyperacute-looking ST-T waves in multiple leads (with greatly reduced R wave amplitude in lateral chest leads) — was whether this was some large acute infarction in progress? BUT — as per Dr. Smith — I thought there were a number of highly atypical findings that were against this being a large acute MI in progress:

• There is marked RAD with an R>S in lead V1. Seen together, these 2 ECG findings suggest possible RVH (For review on "My Take" for the ECG diagnosis of RVH — Please see My Comment at the bottom of the page in the March 6, 2022 post and in the September 1, 2020 post of Dr. Smith's ECG Blog).
• Rather than discrete anatomic localization (as is common with acute MI) — the shape of the abnormal ST-T waves looks remarkably similar in multiple leads.
• There is no reciprocal ST depression.
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• My Impression: After seeing ECG #1 — I was not at all sure what was going on with this patient. While I could not rule out the possibility of a large acute ongoing infarction — I thought it more likely that there was some unusual process operative, including RVH and/or some type of cardiomyopathy.
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• As per Dr. Smith — I was happy to learn that this patient was going to cath! 

The 2nd ECG:

I am unaware of what happened clinically with today's patient — beyond knowing that the cath was negative — acute MI was ruled out — the EF was supernormal at 80% — and there was no suggestion of RVH or cardiomyopathy on Echo. 

Given this clinical follow-up — I found comparison of the post-cath ECG to the initial ECG especially interesting (Figure-1). Compared to ECG #1 — I see the following in post-cath ECG #2:

• The rhythm in ECG #2 is sinus at a slightly slower rate. 
• The frontal plane axis is slightly less rightward. 
• The R wave in lead V1 is slightly more predominant than it was in ECG #1.
• There is no longer a Q wave in lead II — as the tiny but relatively wide initial deflection in this lead is now positive. (The Q waves in leads III and aVF remain).
• There has been an increase in QRS amplitude in leads V3-thru-V6. Considering how tiny the QRS complex was in leads V5,V6 of ECG #1 — I took this increase in amplitude as significant.
• There is less ST elevation in leads II, V2 and V6. But the most remarkable change to me between the 2 tracings — is that ST-T waves overall have considerably less of a "hyperacute-like" appearance.

My Overall Impression of ECG #2 (Compared to ECG #1):

ECG #2 is still an abnormal tracing. There is RAD — a predominant R wave in lead V1 — reverse R wave progression, with still-small QRS complexes in lateral chest leads — and — although the appearance of ST-T waves has improved compared to ECG #1 — ST-T waves still are abnormal in several leads of ECG #2.

• In adults — it is not normal for the R wave in right-sided lead V1 to be taller than the S wave is deep. This is because of left ventricular predominance in adults. As a result — the finding of a Tall R Wave in Lead V1 (ie, R=S or R>S in V1) should prompt the following diagnostic considerations: i) WPW; ii) RBBB; iii) RVH; iv) Posterior MI; v) HCM (Hypertrophic CardioMyopathy); and, vi) Normal Variant (which is a diagnosis of exclusion!).
• That said — None of the common causes of a Tall R in V1 are operative in today's case because the QRS is narrow (ie, No RBBB or WPW) — the normal cath, 80% EF, and lack of any wall motion abnormality is against posterior MI — the normal Echo rules out RVH and HCM — and this ECG is clearly not a "normal variant". (CLICK HERE — for more on my approach to the Tall R in Lead V1).
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• With the normal Echo — I do not have an explanation for the marked RAD. We can not explain the RAD on the basis of LPHB — because this requires a qR pattern not only in lead III, but also in lead II. Whereas I have at times seen unexplained RAD in otherwise healthy young adults — this simply is not something I expect in a 60-year old patient who does not have RVH. 

Final THOUGHTS:

As stated earlier, the "good news" — is that an acute cardiac event was ruled out. My "intellectual curiosity" still wants to know more about WHY this post-cath ECG is still so abnormal-looking despite the negative evaluation. My THOUGHTS:

• It sounds like today's patient was in shock and markedly hypotensive on arrival in the ED (although we do not know the precise etiology — and we do not know the patient's condition at the time that ECG #2 was obtained). 
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• Most ECG parameters show improvement in ECG #2 compared to ECG #1 (ie, less extreme RAD, less ST elevation and less "hyperacute-looking" ST-T waves with increased QRS amplitudes in lateral chest leads). 
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• Low Voltage has been associated with depressed ventricular function (See My Comment in the November 12, 2020 post in Dr. Smith's Blog) — so part of the reason ECG parameters may have improved on ECG #2 could be improvement in the patients condition (with resultant improved myocardial perfusion and therefore improved contractility). But we have no idea if ECG #2 truly represents this patient's "baseline" ECG — or merely an improvement from his ECG when he presented to the ED in shock. Therefore — I'd LOVE to see: i) A prior ECG on this patient when he was well; and, ii) A repeat ECG after a few more days of recovering from his initial illness.
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• Finally — I'd LOVE to see what this patient looks like, as body habitus may at times be responsible for unexpected and unusual ECG findings.