Look at this ST Depression

A healthy 30-something presented with 2 days of chest heaviness.  He had some risk factors for pulmonary embolism, but none for ACS.

There was no SOB.

He had some reasons to be dehydrated.

He had taken a run that day and was symptom free during the run.

He was very well appearing.

Here is his initial ECG:

What do you think?

Interpretation:
Sinus tachycardia with what appears to be ST depression, especially in V2-V5 and ST Elevation in aVR.

But if you look more closely, you'll see that there is a very depressed PR segment (and elevated in aVR).  This is a deep atrial repolarization wave, and can mimic ST depression.  The deepest part of the wave is frequently just after the J-point.

Here I outline the atrial repol wave with my crude pen:

There was initial strong suspicion of ischemia among providers until I pointed this out.


We did a bedside cardiac ultrasound, which confirmed a small RV and hyperdynamic LV:


The patient's heart rate diminished after we put him supine on the cart.  He was orthostatic.  He was given IV fluids and the heart rate came down.

D dimer and 2 troponins were undetectable.  Hemoglobin was normal and there was no evidence of bleeding.

Here is the post hydration ECG:

Completely normal
The atrial repolarization wave is gone.

You might think there is T-wave inversion in leads III and aVF.
But a negative T-wave does not mean there is T-wave inversion.
The T-wave axis, which is measured by the computer, is -12 degrees.
The QRS axis is 6 degrees.
So the QRST angle is only 18 degrees and anything less than 45 is normal.

He was asymptomatic after fluids and was discharged.

Discussion

Atrial repolarization waves are recognized by a downsloping PR segment and are a common cause of false positive stress tests.  They are augmented by tachycardia.

See this paper:
Sapin PM et al.  Identification of false positive exercise tests with use of electrocardiographic criteria: a possible role for atrial repolarization waves. JACC 18(1):127-35; July 1991.  (link is full text)

Link to abstract: http://www.onlinejacc.org/content/18/1/127.abstract


Here is a schematic from my book, The ECG in Acute MI (this is a link to a free pdf)

Learning Points:

1. Recognize the atrial repolarization wave.  It can mimic ST depression.
2. A patient with chest pain who takes a run while symptomatic and feels well during his run is unlikely to have ACS or pulmonary embolism.
3. Look for the QRST angle
4. The problem of the atrial repolarization wave is one of the reasons why the guidelines suggest that measuring ST Elevation should be at the J-point, relative to the PQ junction, NOT relative to the TP segment.

In fact, there is no validated way to measure the ST segment that is highly sensitive and specific for Occlusion Myocardial Infarction.

Here is more on the atrial repolarizaton wave.

Here is more on the QRST angle

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MY Comment, by KEN GRAUER, MD (10/2/2019):

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I love this post for a number of reasons. Dr. Smith emphasizes the important (and often overlooked) point about how the atrial repolarization wave may suggest there is more ST depression than there actually is. This case also provides an excellent opportunity to talk about terminology, and what is and is not likely to be ischemic ST-T wave changes.

• While my “bottom line” interpretation is virtually identical to that of Dr. Smith — I will offer a different approach to how I independently arrived at the same conclusion.
• For clarity — I’ve labeled and put the 2 ECGs in this case in Figure-1.

Figure-1: The 2 ECGs in this case (See text).

MY THOUGHTS: In my opinion — there is ST depression in the initial ECG that was obtained on arrival in the ED ( = ECG #1 in Figure-1).

• The History in this case is of a 30-something man with “chest heaviness” for ~2 days — but apparently without chest pain at the time ECG #1 was obtained. Instead, dehydration was suspected clinically. TRANSLATION: This sounds to me like a low likelihood history for acute ischemia.
• ECG #1 shows definite sinus tachycardia at ~115/minute. Although there is lots of artifact in lead V6 — artifact is minimal for the rest of the tracing. Intervals and axis are normal. R wave progression is normal with transition between leads V3-to-V4. R wave amplitude is generous in the lateral chest leads — but given this patient’s young adult age — this is not necessarily abnormal.
• As per Dr. Smith — the prominent atrial repolarization wave clearly gives suggestion of more ST-T wave depression than there actually is. That said — the RED circles that I have carefully drawn in a number of leads in Figure-1 clearly show that there is some J-point depression (at least in leads V3, V4 and V5). Clearly, the amount of J-point depression in these leads (that extends below the lower boundary of the perfectly rounded RED circles) is minimal — BUT — this has to be considered in light of this patient’s baseline ECG (ie, ECG #2, obtained after rehydration) — in which the horizontal RED lines in leads V3, V4 and V5 show there is some normal baseline ST elevation in most chest leads.
• Regarding assessment of ST-T wave changes — SHAPE is often more important than amount! BLUE arrows in ECG #1 highlight that there is relative flattening of the short ST segments in leads II, V4 and V5. Comparison of the SHAPE of these ST segments in leads II, V4 and V5 of ECG #1 — with the ST segments in these same leads in ECG #2 after rehydration (RED arrows in ECG #2), shows restoration of the normal gradual slow upslope of ST segments in these leads.
• Finally — there is ST segment coving with moderately deep (considering QRS amplitude) symmetric T wave inversion in leads III and aVF — in association with the above-noted ST segment flattening in lead II. NOTE: I could not say for certain at the time I interpreted this initial ECG whether these ST-T wave changes in leads III and aVF were “normal for this patient” — or possibly ischemic ...
• BOTTOM LINE: There are ST-T wave changes in the initial ED ECG ( = ECG #1) at the time this patient presented with sinus tachycardia + clinical dehydration. With the exception of the T wave inversion in leads III and aVF — the above-noted ST-T waves have resolved in ECG #2 after rehydration and slowing of the heart rate.

KEY POINT: The Systematic Approach I favor for the interpretation of each and every ECG you encounter divides the process into 2 separate Steps: i) STEP #1 — Descriptive Analysis = in which you merely describe the findings you see on the tracing without rendering any interpretation! — and, ii) STEP #2 — Clinical Impression = in which you now interpret the ECG findings you noted in Step #1 in light of the clinical situation. (CLICK HERE — if interested in Details of my Systematic Approach to ECG Interpretation).

• In the case of ECG #1 — Descriptive Analysis reveals that there is slight ST segment flattening and depression in a number of leads. In addition — there was ST coving and T wave inversion in leads III and aVF. The specific terminology I use for my description of these ECG findings is that these are nonspecific ST-T wave abnormalities (ie, "nonspecific" because they are not at this point diagnostic for acute coronary disease).
• My Clinical Impression for ECG #1, given the History (ie, a 30-something man with prior chest heaviness, but no current chest pain and clinical dehydration) — was that acute coronary disease was unlikely.

PEARL: The principal finding in ECG #1 was the presence of nonspecific ST-T wave abnormalities in a number of leads. There are actually over 50 causes of ST-T wave changes on ECG — many of which are not cardiac-related. For practical purposes — I suggest memorization of the following LIST of 6 Common Causes of ST-T Wave Changes, as these are the ones you will most commonly encounter. Remembering this LIST will simplify your task of trying to narrow down the most likely causes of the ST-T wave abnormalities you’ve identified on your patient (CLICK HERE — for more detailed discussion of this topic).

• — 1) Ischemia (as in acute coronary disease).
• — 2) LV “Strain” (ie, repolarization changes in association with LVH).
• — 3) Digitalis effect.
• — 4) Hypokalemia/Hypomagnesemia.
• — 5) Rate-related changes (ie, tachycardia!).
• — 6) Any combination of the above!

Regarding this Case: We are told that this patient was clinically dehydrated — but serum electrolyte results were not mentioned.

• Given that this 30-something man apparently had a negative prior medical history — LVH and digitalis use were unlikely.
• His symptoms suggested low-likelihood for acute coronary disease.
• Considering the above 6-Cause LIST — this left us with possibly electrolyte abnormalities (pending lab results) — and/or tachycardia as likely causes of the above noted ST-T wave changes.

The Follow-Up ECG: As noted above — ST-T wave flattening and slight ST depression have resolved in ECG #2. The heart rate has now decreased to a more normal 80-85/minute. Presumably — any electrolyte abnormalities that may have existed have been corrected with rehydration. Thus, there are reasons why the nonspecific ST-T wave changes have normalized.

• ST segment coving with moderate, symmetric T wave inversion persists in leads III and aVF of the post-rehydration tracing. That said — It is not necessarily abnormal to see T wave inversion in leads III and/or aVF, especially when the QRS complex in these leads is predominantly negative (as it is in ECG #2) — and — especially when the ST-T wave in the 3rd inferior lead ( = lead II ) now looks perfectly normal. Therefore, given the low-likelihood of coronary disease in this 30-something male, whose post-rehydration ECG is otherwise completely normal — my Clinical Impression of the T wave inversion that we see in leads III and aVF of ECG #2, is that this is normal for this patient.
• CLICK HERE — if interested in “My Take” on a User-Friendly Approach for remembering which leads in an adult ECG may normally manifest even large Q waves and/or significant T wave inversion.

Our THANKS to Dr. Smith for presenting this case!