Dr. Smith's ECG Blog: A 30-something with Chest pain and SOB

Saturday, March 4, 2023

A 30-something with Chest pain and SOB

A 30-something with h/o DM and HTN presents with CP and SOB and cough.

The ECG is rather classic for pulmonary embolism, and indeed this was a large acute PE.

This is a classic S1Q3T3. Most S1Q3T3 is not due to PE. This one is far more specific, as it is combined with sinus tachycardia and some T-wave inversion in V1-V3. So this entire ECG is very high probability for PE in a patient with acute dyspnea.

T-wave inversion in anterior leads can be Wellens. This is NOT Wellens because the T-wave inversion is DURING the pain (not after -- Wellens' is a syndrome of TWI after an episode of angina is resolved). MOREVER, the morphology of the TWI is just not right for ACS.

S1Q3T3

This is a paper worth reading: Marchik et al. studied ECG findings of PE in 6049 patients who had clinical findings suspicous of PE, 354 of whom had PE. They found that S1Q3T3 had a Positive Likelihood Ratio of 3.7, inverted T-waves in V1 and V2, 1.8; inverted T-waves in V1-V3, 2.6; inverted T-waves in V1-V4, 3.7; incomplete RBBB 1.7 and tachycardia, 1.8. Finally, they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE.

What is an S1Q3T3? Very few studies define S1Q3T3. It was described way back in 1935 and both S1 and Q3 were defined as 1.5 mm (0.15 mV). In the Marchik article, (assuming they defined it the same way, and the methods do not specify this), among patients with suspicion for PE, S1Q3T3 was found in 8.5% of patients with PE and 3.3% of patients without PE.

More on the ECG in pulmonary embolism:

The ECG in this patient has both precordial T-wave inversions AND T-wave inversion in lead III. this is highly suggestive of pulmonary embolism.

Kosuge et al. showed that, when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely than ACS. In this study, (quote) "negative T waves in leads III and V1 were observed in only 1% of patients with ACS compared with 88% of patients with APE (p less than 0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V1 allows PE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads."

See this post for more detail on the ECG in pulmonary embolism.

Still more cases are here.

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My Comment by KEN GRAUER, MD (3/4/2023):

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How good is the ECG for the diagnosis of acute PE? The answer is — it depends! Sometimes the ECG is excellent, in that it immediately tells you "high probability for massive acute PE". At other times — the initial ECG may be suggestive enough to mandate immediate further testing (ie, bedside Echo; chest CT) — albeit not by itself diagnostic. And then there are times when the ECG disappointingly neither rules in nor out a meaningful acute PE.

I completely agree with Dr. Smith in that today's initial ECG is saying, "Treat me as an acute PE until you can prove otherwise!" That said — for discussion purposes, I wanted to focus on a few additional points regarding today's case. For clarity in Figure-1 — I've reproduced and labeled several beats from the initial ECG.

Figure-1: The initial ECG in today's case. I've labeled the 5 beats that are seen in simultaneously-recorded leads V1,V2,V3 — as well as the S1Q3T3 (See text).

How Is the Diagnosis of Acute PE Made on ECG?

As we've discussed many times on Dr. Smith's ECG Blog (See My Comment in the March 28, 2022 post in Dr. Smith's ECG Blog, among many others) — there is no single ECG finding that is diagnostic of acute PE. Instead, the diagnosis of acute PE may be suggested by the presence of at least several of the ECG findings shown in Figure-2 — IF several of these findings are seen to occur in the "right" clinical setting (ie, in association with acute dyspnea consistent with acute PE).

As per Dr. Smith — Today's initial ECG clearly satisfies the above criteria because: i) The patient presented with acute dyspnea; and, ii) ECG #1 shows several of the ECG findings listed in Figure-2 (ie, sinus tachycardia, S1Q3T3, and ST-T wave changes in inferior and anterior leads consistent with RV "strain" ).
While I still had questions about this case given the limited information provided (ie, Was chest pain in this younger adult diabetic from acute PE? Was the ECG ever repeated? Serum troponin?) — The point to emphasize is that today's history and this initial ECG mandate the need for immediate follow-up testing (ie, performing bedside Echo might instantly confirm our suspicion of acute PE).

Additional POINTS:

In my experience — I've seen many clinicians equate an "S1Q3T3" sign to the presence of any 2 (but not all 3) of these components. For this ECG sign to be valid — all 3 components of the S1Q3T3 sign must be present (as they clearly are in Figure-1).
The presence of complete or incomplete RBBB automatically provides an S1 — and often also the T3. As a result — I wonder about the validity of an S1Q3T3 sign as an indicator of acute PE in patients with baseline rbbb conduction abnormalities.
The presence of an S1Q3T3 sign in the absence of a convincing history and at least a couple of the ECG findings noted in Figure-2 — is neither sensitive nor specific for acute PE. Over the years that I interpreted all tracings in an ambulatory care center for 35 medical providers — I would periodically see the presence of an isolated S1Q3T3 in otherwise stable patients without acute dyspnea (and clearly without acute PE).
Acute RV strain is present in ECG #1. That said — When I initially saw today's tracing, I thought there was too much artifact in lead V2 to appreciate true RV "strain". That's because my "eye" focused on the ST-T waves in complexes B, C and D in Figure-1 — in which the baseline is totally erratic and the T inversion that we do see does not line up with the T wave inversion that is clearly seen in lead V1 (Note the discrepancy in the double PURPLE arrows in Figure-1).
Elsewhere in the chest leads — the T wave inversion that we see in lead V3 is shallow — and, rather than clear T wave inversion, the T wave is biphasic (negative-then-positive) in leads V4,V5,V6.
The other place to look for RV "strain" is in the inferior leads. Although the T wave is inverted in lead III — it is not inverted in lead II, and it shows a similar biphasic T wave picture in lead aVF as was seen in the lateral chest leads.
BOTTOM Line: There are clear ST-T wave abnormalities present in multiple leads in ECG #1 — but I was not initially convinced that this ST-T wave appearance was specific for RV "strain".

I then looked closer:

Although there is too much artifact to accurately assess the nature of ST-T wave changes for complexes B, C and D in lead V2 — Complexes A and E in lead V2 do show deep T wave inversion that does line up with the deep T wave inversion that we see in lead V1 (as shown by the double RED arrows in Figure-1). Given that RV "strain" is most typically maximal in anterior leads V1,V2,V3 — the T wave appearance that we see in complexes A and E in lead V2 is clearly suggestive of acute RV "strain".
To EMPHASIZE: The reason I place importance on what the ST-T wave truly looks like in lead V2 — is because apart from sinus tachycardia and the S1Q3T3 sign — none of the other ECG findings listed in Figure-2 would be present if all we had was nonspecific ST-T wave abnormalities. Instead — we do have acute RV "strain" + sinus tachycardia + an S1Q3T3 in a patient with new dyspnea = acute PE until proven otherwise!
P.S.: I would have immediately repeated the initial ECG (with attention to ensure adequate skin contact for the V1,V2 electrodes — which are really the only leads showing significant artifact in today's tracing). I bet a repeat ECG would have been much more clearly diagnostic of acute RV "strain" (and therefore of acute PE).