Tuesday, July 26, 2022

ECG Blog #322 — 71yo with 1 Week of Chest Pain

The ECG in Figure-1 — is from a 71-year old man who presented to the ED (Emergency Department) with a 1-week history of recurrent severe chest and throat painNo prior tracing available.
  • In view of this history — How would YOU interpret the ECG in Figure-1?
  • Is there AV block?

Figure-1: The initial ECG in today's case.

MY Thoughts on the ECG in Figure-1:
I favor beginning with the long lead II rhythm strip.
  • The rhythm in the long lead II rhythm strip is clearly irregular. That said — a majority of beats on this tracing are sinus-conducted, with an upright P wave with constant PR interval in lead II (RED arrows in Figure-2).
  • Sinus P waves are not regular. Instead — every 3rd P wave occurs early (BLUE arrows). The early-occurring P waves are seen to notch their preceding T wave (for the P waves before beats #4 and 7). The premature P wave before beat #10 occurs a little later in the cycle — such that it is more clearly separated from the preceding T wave. 
  • Since every 3rd beat is a PAC (Premature Atrial Contraction) — the rhythm is atrial trigeminy.

  • PEARL #1: Most of the time with the AV blocks — the atrial rhythm will be regular (or at most, no more than slightly irregular when there is sinus arrhythmia). The fact that in Figure-2 — the rhythm in the long lead II rhythm strip is clearly not regular immediately tells us that this rhythm is unlikely to represent 2nd- or 3rd-degree AV block.

Figure-2: I've labeled the P waves from Figure-1 with colored arrows (See text).

Continuing with My Assessment of ECG #1:
The rhythm in Figure-2 is atrial trigeminy. Regarding Intervals — the PR interval and the QTc are both normal. But the QRS complex is wide (I measure 3 little boxes = 0.12 second in duration in a number of leads).
  • QRS morphology is consistent with complete RBBB (Right Bundle Branch Block) because: i) There is an rSR' complex in right-sided lead V1andii) There are wide terminal S waves in left-sided leads I and V6.
  • There is no chamber enlargement.

Regarding Q-R-S-T Changes:
  • Small and narrow Q waves of uncertain significance are seen in leads V5,V6. It is difficult to determine if there is or is not a small q wave in lead III.
  • The question of R wave progression is unimportant given the presence of complete RBBB.

ST-T Wave Abnormalities:
The most remarkable findings in ECG #1 relate to ST-T Wave Changes. Abnormal ST-T wave findings are seen in virtually every lead in this tracing. Some of these are subtle — others less so. But it is important to recognize the totality of these abnormal findings in today's patient who presents with a 1-week history of recurrent chest and throat pain.
  • PEARL #2: Normally with RBBB — there should be at least some ST-T wave depression in lead V1. Although the T wave in this lead is inverted (as it should be) — the shape of the ST segment in lead V1 is slightly coved, and the ST segment is not at all depressed (it actually looks to be slightly elevated). This is not normal!

  • PEARL #3: When there is ST-T wave depression in lead V1 with RBBB — the relative amount of ST depression should be maximal in lead V1. ST depression should then decrease as one moves from lead V1-to V2-to V3 — IF — the reason for the ST depression is purely the conduction defect. This is not what we see in Figure-2 — in which the relative amount of J-point ST depression becomes maximal in leads V3 and V4.
  • Note that the shape of the depressed ST segment in leads V2 and V3 is coved instead of downsloping. Together with the increasing amount of J-point ST depression — this is an ischemic response.

  • There is 1-1.5 mm of abnormal (straightened) ST depression in lateral chest leads V5 and V6. Note the terminal T wave positivity.
  • Similar ST segment straightening with slight depression and terminal T wave positivity is seen in high-lateral leads I and aVL.
  • Nonspecific ST-T wave flattening with slight depression is seen in lead II — and without ST depression in lead aVF.
  • Lead III is interesting — in that the ST segment is distinctly coved, albeit no more than minimally elevated — with symmetric T wave inversion.
  • Finally — there is significant ST elevation in lead aVR.

Putting IAll Together: 
There is a lot going on with this tracing. The rhythm is atrial trigeminy. There is RBBB — and ST-T wave abnormalities consistent with ischemia in virtually all 12 leads.
  • The finding of ST depression in no less than 8/12 leads (I,II,aVL; V2-thru-V6) — with significant ST elevation in lead aVR suggests diffuse subendocardial ischemia. When due to a cardiac cause — this often indicates severe coronary disease (ie, LMain or proximal LAD stenosis — or multivessel disease).
  • Support of the likelihood of multivessel disease is forthcoming from resemblance of ECG #1 to many of the features of Aslanger's Pattern (See below).
  • The history of recurrent severe symptoms of 1-week duration in today's case — in association with the above ECG findings suggests the likelihood that an event (infarction) occurred during this past week.

PEARL #4: There are elements in today's case that closely resemble Aslanger's Pattern (This pattern is very nicely described by Dr. Smith in his January 4, 2021 post). The premise of Aslanger's — is that IF there is inferior MI + diffuse subendocardial ischemia — then the vector of ST elevation will shift rightward. This results in:

  • ST elevation in lead III (as a result of the acute inferior MI) — but not in the other inferior leads (II, aVF) because of the rightward shift in the ST elevation vector.
  • ST depression in one or more of the lateral chest leads (V4,V5,V6) with a positive or terminally positive T wave — but without ST depression in lead V2. (Marked ST depression from multi-vessel coronary disease serves to attentuate what would have been ST elevation in leads II and aVF).
  • ST elevation in lead V1 that is more than any ST elevation in lead V2.
  • There may be more reciprocal ST depression in lead I than in lead aVL (because of the rightward ST vector shift).
  • The only leads showing significant ST elevation may be leads III, aVR and V1 (reflecting the inferior MI + subendocardial ischemia from diffuse coronary disease). 

NOTE: Other than the finding of ST depression in lead V2 — the initial ECG in today's case satisfies the other above-cited features of Aslanger's Pattern
  • I can't help but wonder if the fairly deep, symmetric T wave inversion in lead III represents a reperfusion T wave from recent occlusion.


CASE Follow-Up:
Initial troponin was slightly elevated. The ECG was repeated ~2 hours after the initial tracing (Figure-3). Unfortunately — additional details of this case are lacking.
  • How would you interpret the repeat ECG in Figure-3?

Figure-3: Comparison of the initial ECG — with the repeat ECG done ~2 hours later. Unfortunately — clinical details are lacking regarding the nature of the patient's symptoms during this 2-hour time period

Comparison of the 2 ECGs in Today's Case:
The rhythm in ECG #2 is similar to that in the initial ECG ( = sinus rhythm with PACs). Overall QRS morphology is also similar in the 2 tracings.
  • There is less ST segment depression in leads V2-thru-V5 of ECG #2 compared to the initial tracing.
  • In lead III — there is now a definite Q wave and slight-but-real ST elevation. There is no longer any T wave inversion.
  • The flat ST depression with terminal T wave positivity that was seen in high-lateral leads I and aVL of ECG #1 — has been replaced by mirror-image opposite T wave inversion (opposite in shape, compared to the ST elevation in lead III). There is no longer terminal T wave positivity.

MY Impression of ECG #2:
I wish we had more follow-up information on this case. I suspect the following:
  • The new ST elevation in lead III — with reciprocal (mirror-image opposite) ST depression in leads I and aVL — to me suggest reocclusion of the RCA (Right Coronary Artery). Remember that with Aslanger's Pattern — ST elevation of inferior infarction may only be seen in lead III.
  • Clear reduction in the amount of ST depression in leads V2-thru-V5 — that occurs in association with signs of RCA reocclusion — suggests to me that ECG #2 may represent the phenomenon of "pseudo-normalization", in which the ECG looks "improved" because previously depressed ST segments are on their way toward ST elevation.

ADDENDUM (7/26/2022):
I have just received additional follow-up on this case. Cardiac cath was done — and revealed total occlusion of the LCx. The RCA was hypoplastic and showed 80% stenosis. The LMain was patent — and there was insignificant disease in the LAD. Ejection fraction ~42%. Successful PCI was performed (Figure-4).

Figure-4: Cardiac Cath — showing total occlusion of the LCx (LEFT). Successful PCI restoring flow to the LCx (RIGHT).


Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.


Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

  • ECG Blog #204 — Reviews a user-friendly approach for diagnosis of the Bundle Branch Blocks.

  • ECG Blog #186 — and ECG Blog #236 — for review on the basics of 2nd-degree AV Block.

  • ECG Blog #258 — Reviews the concept on how to "date" an infarction (and also introduces the concept of Aslanger's Pattern).
  • ECG Blog #271 — and ECG Blog #250 — Review the concept of diffuse subendocardial ischemia.
  • ECG Blog #142 — Presents another case for discussion on how to "date" an infarction.

  • ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "culprit artery". NOTE: Figure-5 in the Addendum of this blog post illustrates the essentials for identifying an isolated posterior MI.

  • ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post).
  • ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).

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