Syncope and ST Elevation on the Prehospital ECG

A 75 yo with h/o CAD, CABG, and HFrEF presented after a syncopal episode.  There was no prodrome and no associated symptoms such as SOB or CP. 

The medics recorded an ECG:

There is STE in V1-V3 and aVL, with reciprocal ST depression in II, III, aVF.
The medics were worried about STEMI, as it meets STEMI criteria.
What do you think?

On arrival, BP was 150/80, with a pulse of 80.  An ECG was recorded:

Now you can see what the medics could not: The QRS is enormous. There is LVH.  
The ST Elevation is due entirely to LVH.
The QRS duration is 118 ms, so by definition it is not Left Bundle Branch Block (which must be 120 ms at a minimum and is usually longer)
Thus, LVH on the ECG does not always correlate with anatomic LVH.
Nevertheless, high voltage does correlate with abnormal ST segmentsThe S-wave in V2 is 50 mm; STE is 2.5.  Ratio = 0.05, which is normal.
LVH PseudoSTEMI

On further history, he had been walking around all day in the heat without drinking.  The syncope occurred during micturition.

(Head CT and CT pulm angiogram were done and were both negative)

So this is simple, right?

Not so fast.

The first troponin I returned at 0.016 ng/mL, but the second 0.208 ng/mL. 

ECG 3 hours later was unchanged

He was not started on heparin as type II MI was favored over NonSTEMI as the etiology of his troponin elevation.  

He was admitted for monitoring, as his risk of a ventricular dysrhythmia as cause of the syncope is high (very high due to HFrEF and ischemic cardiomyopathy).

Troponin profile

Due to these troponins which are typical for an NSTEMI, a formal echo was done:

Decreased left ventricular systolic performance, moderately-severe.

The estimated LV ejection fraction is 35%.

Regional wall motion abnormality-distal septum and apex.

Left ventricular enlargement, severe.


--There is no mention of concentric hypertrophy, but only severe enlargement (very different!) 
--Thus, LVH on the ECG did not correlate with anatomic LVH.

ADDITIONAL REMARKS

Evidence for dilated left ventricle with regional dysfunction in the LAD distribution. Markedly dyssynchronous septal motion consistent with LBBB activation pattern. No previous study for comparison.

Clinical Course:

- He had no events on cardiac monitoring overnight.
- He rehydrated and had no orthostatic symptoms prior to discharge, ambulated well.

- He denied chest pain or dyspnea throughout.

He was not interested in remaining hospitalized for further cardiac monitoring or inpatient EP consultation as he felt well, was convinced dehydration was the reason for his syncope, and he adamantly wanted to go home. 

Discussion

Thus, no further ECGs were recorded and there was no angiogram or stress test or CT coronary angiogram.  Acute MI does not often present with syncope alone, without any other symptom, so the pretest probability of acute MI is low.

However, the troponins are high and, in my opinion, the data above does not rule out the possibility of type 1 MI.  There were very elevated troponins without a significant known stress (which might cause a type 2 MI).  The troponins are NOT consistent with STEMI (OMI), which typically has a troponin I of at least 5 ng/mL.  Nevertheless, I don't think a thrombosis related type I MI was ruled out here simply because the patient refused further evaluation.

Assessment: syncope due to combination of micturition, dehydration, and poor LV function

Fortunately, follow up confirmed that he did well over the long term.

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MY Comment by KEN GRAUER, MD (6/20/2020):

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This case has some similarities to the February 6, 2020 post on Dr. Smith’s ECG Blog. IF you missed the KEY Findings on the pre-hospital ECG of today’s case — Please take another look at My Comment at the bottom of the page of that February 6, 2020 post.

• In the interest of not repeating my detailed discussion from February 6 — I focus my comments here on specifics regarding the 2 ECGs in today’s case. For clarity — I’ve put them together in Figure-1.

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

My THOUGHTS on ECG #1: It’s important to immediately recognize WHY I have added the 2 small RED circles to ECG #1 ( = the pre-hospital ECG).

• There is a limit to the amount of voltage that prehospital ECGs in most EMS systems are able to display. As a result — QRS amplitudes are automatically truncated once they exceed that limit. This explains the space between ascending and descending limbs of the QRS complex in leads II and III of ECG #1 (within those small RED circles in these leads).
• DO YOU SEE where QRS amplitude has also been automatically truncated in each of the anterior leads of ECG #1?

As per Dr. Smith — the result of this “automatic truncation” of S wave amplitude in leads V1, V2 and V3 of ECG #1 becomes immediately apparent once we compare the pre-hospital ECG — to ECG #2 (which is the initial ECG done in the ED):

• Note in Figure-1 the tremendous increase in QRS amplitude in virtually every lead of ECG #2 compared to ECG #1!

QUESTION: Just HOW LARGE are QRS amplitudes in ECG #2?

ANSWER: It can sometimes be very difficult to determine QRS amplitude when there is overlap of R waves or S waves from one lead to the next. In ECG #2 — there is actually a place on the tracing where there is overlap of QRS complexes in 3 leads! (RED, GREEN and BLUE lines in Figure-2, showing overlap of R waves and S waves from leads V2, V3 and from the long lead II rhythm strip below).

• The S wave in lead V2 appears to be 48 mm (RED lines in lead V2).
• The S wave in lead V3 appears to be 20 mm (GREEN lines in lead V3).
• The R wave in the long lead II appears to be 31 mm (BLUE lines in the long lead II rhythm strip).
• The “easy solution” for resolving the problem of excessive QRS amplitude causing overlap of complexes — is to record the ECG at HALF standardization. Unfortunately, this option might not be available for pre-hospital tracings.

Figure-2: I’ve colored the QRS complex in leads V2, V3 and in the long lead II in RED, GREEN and BLUE, respectively — to illustrate the actual size of the QRS complex in each of these leads. (See text).

This leaves us with the challenge of assessing the ST-T wave changes in ECG #2. In addition to the dramatically increased QRS amplitude that we see in virtually every lead — there is ST segment elevation in leads V1 and V2 (as well as ST segment coving with slight T wave inversion in lead aVL) — and, ST segment flattening with slight ST depression in most of the other leads (Figure-3).

• As per Dr. Smith — now that we see how very large the S waves really are in each of the anterior leads of ECG #2 — the several mm of ST elevation that we see in leads V1 and V2 do not look to be disproportionately tall.
• ST-T wave changes of LV “strain” in response to marked LVH are most commonly seen in one or more of the lateral leads (ie, leads I, aVL; V4,V5,V6). In its most extreme form — these changes manifest as asymmetric ST depression (ie, the ST segment descends slower than it rises) — but, less pronounced forms of this phenomenon, that I call an LV “strain equivalent” — are often seen. In a patient with underlying heart disease who satisfies voltage criteria for LVH — the finding of either LV “strain” or a “strain equivalent” greatly increases the specificity of the ECG for diagnosing true LVH (Figure-4).
• As I explained and illustrated in detail in the February 6, 2020 post — Use of the Mirror Test (ie, inverting the QRST complex in lead V1) may facilitate recognizing what the shape of LV “strain” may look like in a right-sided lead (such as lead V1 or V2). As shown in the insert for lead V1 in Figure-3 of today’s case — the Mirror Test inverted image of the QRST complex in lead V1 looks exactly as you’d expect for a patient with LVH + “strain” (ie, increased R wave amplitude with asymmetric ST depression having a slow downslope, and a more rapid terminal rise). Lead V2 in Figure-3 shows a similar picture consistent with LVH + “strain” in this right-sided lead.
• Many other leads in Figure-3 manifest the ST segment flattening with slight depression consistent with a “strain equivalent” pattern.
• Echo confirmed that the above ECG findings in today’s case were the result of severe LVH.

Figure-3: Another look at ECG #2 — with the insert showing a mirror-image view of the QRST complex in lead V1 (See text).

Figure-4: Illustration and description of LV “strain” and a “strain equivalent” pattern (See text).

There are many ECG criteria for the diagnosis of LVH. I list those that I favor in Figure-5 — and discuss in detail my approach to the ECG diagnosis of LVH at THIS LINK.

• There is a rough (but far-from-perfect) correlation between the relative size of the QRS complex on ECG — and the degree of LV chamber enlargement. Clinically — One can glean insight from the ECG as to the likely relative amount of LV chamber enlargement based on: i) HOW MUCH voltage is increased by, according to criteria in Figure-5; and, ii) the presence and extent of ST-T wave changes consistent with either “strain” or a “strain equivalent” (as described in Figure-4).

One Final Point (that is Beyond-the-Core): Take one last look at Figure-1. Can you explain the bizarre rsR’S’ appearance of the QRS complex in lead I of ECG #1 in Figure-1?

MY Thoughts: The amount of voltage in ECG #1 is huge! QRS amplitude is increased by as much as you are likely to see. In addition — the QRS complex looks wide in ECG #1 (I measured 0.12 second). Some of this increase in QRS width may be attributable to massive LVH (ie, it will take longer for the electrical impulse to traverse a larger and thicker left ventricle). But it is also possible that we are seeing an incomplete form of LBBB. Occasionally with complete LBBB — there may be relatively more conduction block in the posterior compared to anterior hemifascicle — and in the presence of marked LVH, this might produce the unusual changing-vector deflection we see in lead I of ECG #1.

• I believe the Echo finding of “markedly dysynchronous septal motion, consistent with an LBBB activation pattern” supports my theory.
• Of interest — Lead I on the initial ECG from the ED = ECG #2 (which was done a bit after the prehospital ECG #1 was done) — no longer shows this unusual 4-phase QRS deflection in lead I. I have seen similar occurrence in patients with LBBB — in which sometimes there may be more or less right axis deviation in association with the LBBB from one-day-to-the-next (presumably due to a changing relative difference in the degree of block in one of the hemifascicles).

BOTTOM Line: Memorize the ECG pattern you see in ECG #1 of Figure-1. You WILL encounter this pattern again (probably a number of times!) — and it is important to: i) Realize that QRS amplitude is automatically truncated by many prehospital ECG machines; and, ii) In view of this automatic truncation of QRS amplitude — the shape of ST elevation seen in leads V1, V2 and V3 of ECG #1 will most often not be the result of acute anterior STEMI, but rather reflect LV “strain” from marked LVH in these right-sided leads.

• Our THANKS to Dr. Smith for presenting this case.

Figure-5: Criteria I favor for the ECG diagnosis of LVH (See text).