Dr. Smith's ECG Blog: What is going on in V2 and V3, with a troponin I rising to 1826 ng/L at 4 hours?

I was reading EKGs on the system before a shift, and saw this one:

What do you think?

I was worried that the ST depression and T-wave inversion in V2 and V3 might be posterior OMI. I went to the chart and found that the patient was a sepsis patient with hypotension and a K of 3.0. There was no chest pain. So I thought it probably is not posterior OMI and I just moved on and kept reading EKGs.

Later, I was working in the ED and a patient was moved from a regular room to the critical care area due to recurrent hypotension. The patient was now under my care. In reviewing the case, I saw the ECG and recognized it as the same one. By this time, 2 troponins had returned, the first at 40 ng/L and the 2nd 2 hours later at 803 ng/L, and then a third at 1826 ng/L at 4 hours.

Now I was worried that there was indeed a posterior OMI. But she still had no chest discomfort at all and did have every reason to have a type 2 MI (due to hypotension). In reviewing her chart more, I found that she had had what was deemed a type 2 MI 6 weeks prior. No angiogram was done at that time.

Here is the ECG from that visit:

Nothing Diagnostic, just a lot of nonspecific ST-T abnormalities.

There is, however, a very peaked P wave in lead II (a "peaked P pulmonale").

This suggests that there is pulmonary hypertension and thus possibly RVH.

However, there is no significant right axis deviation and no large R-wave in V1, which argues pretty strongly against RVH.

As Ken states below, there are also pronounced S-waves in V5 and V6; this is another sign of RVH.

We recorded another ECG 3 hours after the first:

The findings in V2 and V3 persist.

I looked through her chart and found a formal echo from the last visit showing "Severe right ventricular enlargement and decreased RV systolic function".

So we did a bedside cardiac ultrasound. Here are 4 views (sorry, I used my iPhone to take videos of the computer screen):

These all show a very large RV and an LV which appears to have good function. I could not see a posterior wall motion abnormality.

More thoughts now on the EKG: These ST-T waves are very typical of RV hypertrophy, but such ST-T abnormalities of RVH are usually are seen in the setting of right axis deviation and large R-wave in V1, so I was not convinced. On the other hand, from the previous echo 6 weeks prior, I had formal echo evidence of RV enlargement.

At this point, I was pretty sure that there was not posterior OMI but that this was RV hypertrophy. But I wasn't certain.

I called cardiology to get a formal echo.

They agreed about formal echo. Here is the result:

--Small, under-filled left ventricular cavity.

--Normal left ventricular systolic function with an estimated EF of 60%.

--No regional wall motion abnormality.

--Septal flattening during systole and diastole consistent with pressure and volume overload.

--Severe right ventricular (RV) enlargement and decreased RV systolic function.

--Right atrial enlargement, severe.

--Severe tricuspid regurgitation.

--The estimated pulmonary artery systolic pressure is 31 mmHg + RA pressure.

--Based on the appearance of the IVC, the estimated RA pressure is elevated.

Troponin peaked at 2914 ng/L

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Comment by KEN GRAUER, MD (2/12/2023):

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Among the most challenging of ECG diagnoses to make is RVH (Right Ventricular Hypertrophy). By saying this — I am not referring to obvious cases of ECG RVH — in which the QRS is of normal duration (ie, No RBBB and no WPW) — and there is marked RAD (Right Axis Deviation) + a predominant R wave in lead V1.

KEY Point: The extreme ECG findings of marked RAD and predominant R wave in lead V1 are usually not found in adults with RVH — until late in the course, and sometimes not even then. Instead — I am referring to less obvious, but still clinically significant forms of RVH that are all-too-easy to overlook!

Consider the following:

RVH is much easier to diagnose in infants and young children than in adults. This is because the relative size (and mass) of the RV (Right Ventricle) compared to the LV (Left Ventricle) — is much greater in infants and young children compared to adults. In contrast, by the time adulthood is reached — the normal LV may be up to 3X as thick (with up to 10X the mass) of the normal RV. As a result — a marked increase in RV size is usually needed in adults — before a predominant R wave will be seen in lead V1.
In contrast — an R>S ratio (ie, R wave height greater than S wave depth) in lead V1 remains a common and normal finding in children up until ~5 years of age!
Similarly (ie, because of the normal LV predominance) — marked RAD in the frontal plane is a relatively late sign of RVH in adults.

PEARL #1: Think of the ECG diagnosis of RVH as a “detective” diagnosis. No single clue solves the mystery. Instead — determination of RVH is made by deduction (ie, by identifying a combination of ECG findings in a patient with a clinical history consistent with RVH).

I’ve reviewed My Take on the ECG diagnosis of RVH on a number of occasions in Dr. Smith’s ECG Blog (See My Comment at the bottom of the page in the March 6, 2022 and September 1, 2020 posts, to name just 2).
As review — my user-friendly summary of ECG RVH appears in the ADDENDUM below (in Figures-3 thru -6).

How Does this Apply to Today’s Case?

For clarity in Figure-1 — I’ve labeled the initial ECG shown in today’s case.

PEARL #2: As is often the case — the History is KEY! Acute posterior OMI would be a prime concern for the ECG in Figure-1 — IF the patient presented with cardiac-sounding chest pain. But today's patient had no chest pain.
Alternatively — the symmetric T wave inversion in leads V2 and V3 in today’s initial ECG could be perfectly consistent with RV “strain” in a patient with RVH — IF: i) Other ECG findings consistent with RVH were present; and, ii) The patient’s history was consistent with pulmonary disease or other entity likely to be associated with RVH.

Other ECG findings consistent with RVH in Figure-1:

The Axis: While frank RAD is not present — the normal QRS complex in lead I is positive. Low amplitude of the R wave in lead I of Figure-1 — in association with an S wave of equal size to the R wave in this lead is not a usual finding.
Relatively Low Voltage: While strict criteria for low voltage are not present (ie, All 6 limb leads ≤5 mm) — overall QRS amplitude looks reduced in the limb leads of Figure-1.
RAA (Right Atrial Abnormality): The tall, peaked and pointed P wave in each of the inferior leads (≥2.5 mm tall in lead II) — satisfies ECG criteria for RAA. There is only 1 condition in medicine that produces right atrial enlargement without also producing RVH. That condition is tricuspid stenosis, which is rare. Therefore, the ECG finding of RAA that is not the result of slender body habitus — often provides an important indirect clue to the presence of RVH.
Persistent S Waves: R wave amplitude normally increases as one moves across the precordial leads (as electrical activity moves toward the left where the larger LV lies). R wave amplitude usually peaks in V4 or V5 — and then drops off (in V5,V6). Normally, there is not any S wave at all in V5,V6 — since by this time in the depolarization process, all electrical activity is traveling leftward. If more than tiny S waves are still present in V5,V6 — this may be the result of significant ongoing rightward activity.
A qR Pattern in Lead V1: While the height of the R wave in lead V1 of Figure-1 is not overly tall — this terminal R wave (that at least equals depth of the S wave in lead V1) is not normally seen. In a patient with RVH — the finding of a qR pattern has been closely correlated with pulmonary hypertension.

To EMPHASIZE: In isolation — None of the ECG findings mentioned above would be diagnostic of RVH. However, when taken together — the combination of these ECG findings is at least suggestive of RVH, pending review of the patient’s chart for additional information.

As per Dr. Smith — Chart review and repeat formal Echo confirmed marked RVH with pulmonary hypertension.

Figure-1: I’ve labeled subtle findings potentially consistent with RVH — from the initial ECG in today case.

Beyond-the-Core: Looking Closer at the qR in Lead V1

Technically — one might be tempted to call the qR pattern that we see in lead V1 of Figure-1 as consistent with IRBBB (Incomplete RBBB) — because terminal S waves are seen in lateral leads I and V6 of both tracings. My preference (given the totality of ECG findings) — is to attribute this qR pattern to RVH with pulmonary hypertension, rather than to postulate a conduction defect. That said — it is true that complete and/or incomplete RBBB is a common accompaniment of RVH.
PEARL #3: There is a physiologic reason why pulmonary hypertension from advanced RVH may result in a qR pattern in lead V1 (Figure-2).

Figure-2 (from my ECG Blog #248 — adapted with permission from Dr. R Balasubramanian):

LEFT: The circular configuration of the normal left ventricle in this short-axis view — with corresponding rS morphology in lead V1 (WHITE arrow illustrating septal depolarization that is initially oriented toward lead V1).
RIGHT: Increased RV pressure (with associated RV dilatation) is transmitted to the interventricular septum, and produces a "D-shaped" deformity of the LV (as seen here, in this short-axis view). Flattening of the septum in this manner alters the direction of initial septal activation, that is now oriented away from lead V1 (WHITE arrow), thereby producing the qR pattern in lead V1 that is seen with RVH + pulmonary hypertension.
Clinical NOTE: As a consequence of severe RVH with associated pulmonary hypertension — there may progressive RV dilatation. This often leads to significant TR (Tricuspid Regurgitation). This sequence of events further explains the qR pattern seen in lead V1 — because severe TR leads to marked clockwise rotation of the right ventricle (which accounts for a change in anatomic orientation of the interventricular septum). This fulfills the clinical adage in these patients that, "qR = TR" (ie, a qR pattern in lead V1 is very often associated with severe tricuspid regurgitation).