Wednesday, June 17, 2020

A 60-something has chest tightness, palpitations, and ST depression V1-V3

A 60-something has chest tightness, palpitations.  Charts showed a history of some mitral regurgitation and an enlarge left atrium, as well as hypertension treated with a thiazide diuretic.

A prehospital ECG showed ST Depression in V1-V3 and the medics were concerned for posterior STEMI.

On arrival, the patient was in minimal distress, stated that he "always has chest tightness" but that his "heart started jumping around" one hour prior.

Pulse was 128 and irregular, BP was 141/75.

Here is the 12-lead:
Atrial Fibrillation with slightly rapid response.
ST Depression maximal in V2 and V3.
What do you think? What do you want to do?

ST Depression in V2, V3 is most often due to "posterior" transmural ischemia (now called "lateral" by a convention that I disagree with because posterior and lateral MI are different on the ECG).

However, sometimes it is due to subendocardial ischemia.  Subendocardial ischemia "does not localize", meaning that if this is subendocardial, you cannot say for certain that it is of the anterior wall.  Furthermore, subendocardial ischemia usually has an STD vector towards II and V5, with a reciprocal STE vector towards aVR.

Atrial Fib with RVR is often associated with subendocardial ischemia, so I thought this might very well NOT be posterior MI, but rather subendocardial ischemia.  Usually such ischemia from atrial fibrillation is with a very fast ventricular response (~150); here it is not so fast.

A bedside echo was unable to find any wall motion abnormality, but these are notoriously insensitive.

A K returned at 2.7 mEq/L.  Could this STD be due to hypokalemia?

Hypokalemia can mimic posterior MI since there is ST depression with an upright U-wave.  Is this ST depression due to the low K?

No, this did not fit for the following reason:

The major difference between STD in V2-V3 from  hypoK vs. posterior MI is that the QU interval is much longer than the QT of posterior MI.  Here is an example of hypokalemia mimicking posterior MI:
This is hypokalemia (K = 2.0) mimicking posterior MI
The upright wave in V2-V4 is a U-wave
Note the very long QU interval.

Case continued

So this ECG is not due to hypokalemia, but due to either posterior transmural ischemia, or subendocardial ischemia.

For the fun of it, we recorded posterior leads V7-V9, and there was no ST Elevation, which does not rule out posterior MI, but does make it less likely.

How do we make the distinction?  We slow the heart rate, either with AV nodal blocker or cardioversion, and see what happens.

So we electrically cardioverted to sinus rhythm, and recorded another ECG:
Now there is only trace residual ST depression.
This is good evidence that it was all rate related.

So we decided this was not acute coronary syndrome.

The patient was admitted to the hospital.

He ruled out for MI.

Here was a TEE result from one month prior:
Left atrial enlargement .
Normal left ventricular cavity size.
Normal estimated left ventricular ejection fraction .
No wall motion abnormality 

Atrial fib was attributed to the combination of mitral regurgitation with a large lef atrium and hypokalemia (which was due to thiazide diuretics for HTN).

He was discharged on a new anticoagulant, a monitor patch for 2 weeks, and a beta blocker, in sinus rhythm.

Learning Point:

When there is ST depression and atrial fibrillation with RVR, it is very useful to cardiovert if possible, or slow AV conduction, before assuming that the ST depression is a result of ACS.

MY Comment by KEN GRAUER, MD (6/16/2020):
Interesting case presented by Dr. Smith — regarding this 60-something year old man who presented with chest tightness (that he has frequently had before)  and new-onset palpitations in association with ECG #1, which I have reproduced in Figure-1.
  • Dr. Smith has covered in his discussion above the details regarding the ST segment depression that was maximal in leads V2 and V3 on the initial ECG ( = ECG #1).
  • As per Dr. Smith — the fact that the ST depression in the chest leads of ECG #1 in large part resolved following electrical cardioversion (See ECG #3 in Figure-1) — strongly supported Dr. Smith’s conclusion that rate-related subendocardial ischemia was the most probable cause of the ST depression seen in the original tracing.
  • We are told that this patient was hypokalemic (serum K+ = 2.7 mEq/L) at the time ECG #1 was obtained. We are also told that this patient was admitted to the hospital — but we are not given additional information.
  • - - - - - - - - - - - - - 
  • NOTE (6/17/2020): At the time I wrote my comments below — I was not aware of this patient's prior medical history. All that I knew, was that this patient presented with chest tightness and palpitations — and that he "always has chest tightness". Please consider the Questions I pose and my Comments below from that perspective.

Figure-1: The initial ECG in today’s case, obtained at the time this 60-something year old man presented in fairly rapid AFib — and — the 3rd tracing shown above, which was obtained following electrical cardioversion (See text).

QUESTIONS: In the interest of “digging deeper” — WHAT are YOUR clinical impressions about this case? While true that emergency management has been successfully accomplished in this case (ie, The patient’s rapid AFib has been cardioverted — and you’ve essentially ruled out acute ischemic heart disease) — there is an important ECG finding relevant to this case that has not been mentioned.
  • WHAT is that ECG finding?
  • Beyond-the-Core: WHY does beat #10 in ECG #1 look different in simultaneously-recorded leads aVR, aVL, aVF and lead II, compared to other beats in these same leads?

ANSWERS: Reading this case left me with a number of clinical questions:
  • Was this the 1st episode of AFib in this 60-something year old patient? Although implied in the brief history we are given that this is this patient’s 1st episode of AFib — the fact that he “always has chest tightness” might imply frequent intermittent episodes of AFib in the past.
  • PEARL #1 — Holter studies have shown that the overwhelming majority of AFib episodes are not associated with symptoms. As emergency providers — we see those AFib episodes that are associated with symptoms — but at least half (if not more) of all patients with AFib have PAF (Paroxysmal AFib), in which AFib episodes recur at some frequency — and a majority of those recurrences appear to be asymptomatic. Awareness of this clinical reality becomes especially important when contemplating long-term anticoagulation questions.
  • PEARL #2 — Rapid SVTs (including AFib) are a potential cause of chest discomfort. As a result — I’d want to know IF this patient’s palpitations and his “chest tightness” both rapidly resolved as soon as sinus rhythm was restored! IF so — this would make it that much more likely that this 60-something year old man was having frequent episodes of PAF!
  • The ECG finding that should be recognized in both of this patient’s tracings is the markedly increased R wave amplitude that begins as early as in lead V2. While true that posterior infarction sometimes results in early transition with increased anterior R wave amplitude — it generally does not produce R waves as predominant as are seen in lead V2. This overly tall R wave in lead V2 is not a normal finding — and it may be a marker of underlying heart disease that could be a contributing cause of this patient’s AFib. A formal Echo needs to be part of this patient’s hospital evaluation.

Beyond-the-Core: I label the last clinical point that I want to discuss as “Beyond-the-Cord” — because although it has no bearing on the outcome of this particular case — awareness of the Ashman phenomenon is an important clinical concept in emergency arrhythmia interpretation.
  • The basic tenet of the Ashman phenomenon — is that conditions for aberrant conduction are set up by an interplay between the coupling interval from one beat to the next — and the preceding R-R interval (with the length of this preceding R-R interval determining the duration of the subsequent refractory period). For example, in ECG #1 — the coupling interval for beat #10 is the R-R interval between beats #9-to-10. The shorter this coupling interval is — the greater the chance that beat #10 will fall within the RRP (RelativeRefractory Period) of beat #9 (and the greater the chance that beat #10 will conduct with aberration).
  • The “easy way” to think about the Ashman phenomenon — is to remember that aberrantly-conducted beats tend to follow longer pauses. The reason for this, is that the relatively longer pause between beats #8-to-9 in ECG #1 will prolong the RRP of beat #9.
  • NOTE: Both factors (ie, the coupling interval and the preceding R-R interval) are operative in determining whether a given early-occurring beat conducts normally or with aberration.
  • In ECG #1 — the shortest coupling interval in the entire lead II rhythm strip is between beats #3-to-4. Although beat #4 does conduct with slight aberration (best seen in lead III for beat #4) — the reason a much greater degree of aberration is seen for beat #10, is that the preceding R-R interval (ie, the R-R interval between beats #8-to-9) is much longer than the R-R interval preceding beat #4.
  • In ECG #1 — the longest preceding R-R interval is between beats #13-to-14. But despite the length of this pause between beats #13 and #14, the reason beat #15 does not conduct with aberration is that its coupling interval (ie, the R-R interval between beats #14-to-15) is not nearly as short as the coupling interval of beat #10.
  • NOTE: This interplay between preceding R-R interval and coupling interval of the early-occurring beat is not always exact. It clearly is less than perfect when assessing early-occurring beats in AFib, since concealed conduction may reduce reliability of predicting the RRP from the surface ECG. But, awareness of the Ashman phenomenon is helpful — and with practice allows you to “eyeball” an AFib rhythm and immediately suspect that the widest, most different-looking beat (which is beat #10) is likely to be aberrantly conducted (instead of a PVC) — because the coupling interval of beat #10 is short and this beat is also preceded by a relatively longer pause.
  • CLICK HERE for a more detailed explanation of the Ashman phenomenon.
  • For a more thorough appreciation of the complex relationship of the Ashman phenomenon in AFib — CLICK HERE

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