Friday, December 23, 2022

ECG Blog #352 — Chest Pain 1 Week Ago ...

The ECG in Figure-1 was obtained from a woman in her 80s — who presented with a history of having had 1 episode of chest pain during the previous week. No chest pain since.

  • Given this history — What happened?
  • How would YOU interpret the ECG in Figure-1?

Figure-1: ECG obtained from a woman in her 80s — who presented with 1 episode of chest pain during the previous week. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:
The mechanism of the rhythm in ECG #1 is sinus (ie, P waves are present and upright in lead II — with a constant PR interval throughout the long lead II rhythm strip). There is slight variability of the R-R interval — with an overall rate of ~60/minute.
  • The PR interval is markedly prolonged (ie, to ~0.40 second) — so this is sinus arrhythmia with 1st-degree AV block.

Regarding the other intervals — the QRS is not wide — and the QTc does not appear to be prolonged. The frontal plane axis is normal at about +40 degrees. There is no definite sign of chamber enlargement.

Regarding Q-R-S-T Changes:

  • Small and narrow Q waves of uncertain significance are seen in each of the inferior leads
  • There may in addition, be tiny septal q waves of no significance in the lateral chest leads.

  • R wave progression in the chest leads manifests a normal "zone" of transition (in that the R wave becomes taller than the S wave is deep between leads V2-to-V3). That said — this transition is more abrupt than usual, with the R wave fairly suddenly becoming predominant in lead V3.

Regarding ST-T Wave Changes:
  • In the inferior leads — there is slight ST elevation in lead III — ST-T wave flattening in lead II — and the suggestion of ST coving with slight-but-real terminal T wave inversion in leads III and aVF.
  • That these findings are "real" — is supported by recognition of reciprocal changes in high-lateral leads I and aVL (in which there is ST segment flattening with slight depression and terminal T wave positivity).

  • PEARL #1: Interpretation of the limb lead changes in today's tracing is challenging — because of baseline artifact and resultant variation in ST-T wave morphology between the 2 beats that are seen in each of the limb leads. That said — What counts, is that although the ST-T wave appearance for each of the beats in these 5 limb leads manifests some variation in morphology — the overall (ie, "Gestalt") appearance of ST-T waves in these limb leads is consistent with a common "theme", which is — that in a patient reporting a recent episode of chest pain that has now resolved — these findings suggest a recent event that now manifests reperfusion T waves in the inferior leads.

  • PEARL #2: Given how common it is for acute or recent inferior OMI to also manifest ECG changes of posterior OMI — I immediately focused my attention on assessing for such changes in the anterior chest leads. Recent posterior OMI is suggested in ECG #1 by: i) Distinctly abnormal ST segment flattening in the anterior chest leads; ii) Surprisingly tall, symmetric T waves in leads V1-thru-V4 (maximal in V2,V3) that are consistent with posterior reperfusion T waves; and, iii) Abrupt development of a predominant R wave in lead V3 (See ECG Blog #351for more on these topics).

  • Completing our assessment for ST-T wave changes — Note that ST segment flattening with slight ST depression continues across the precordium to extend to the lateral chest leads (ie, leads V4,V5,V6).

  • PEARL #3: As discussed most recently in ECG Blog #350 — there is T wave "imbalance" in the chest leads. That is, when T waves in all 6 chest leads are positive — the T wave in lead V1 is not normally taller than the T wave in lead V6 (as it is in Figure-1). This finding sometimes provides a clue to recent OMI (especially from a LCx culprit artery).

ECG #1 — Putting IAll Together:
The series of events and ECG findings described above can be put together to formulate a consistent story:
  • The history in today's case (ie, of an older woman who describes an episode of chest pain days earlier — but which has now resolved)is consistent with a recent event.
  • Acute coronary occlusion is often followed by spontaneous reopening of the "culprit" artery. Clinically — these events are suggested by resolution of chest pain at a similar time that reperfusion T waves are seen on ECG. The presence of such reperfusion T waves in the inferior and posterior areas of ECG #1 — suggest that the "culprit" artery was either the RCA (Right Coronary Artery) or the LCx (Left Circumflex). Although a majority of individuals manifest RCA-dominance — the finding of chest lead T wave "imbalance" favors the LCx as the "culprit". KEY Point: Regardless of what the culprit artery turns out to be — the above-described sequence of events is consistent with the spontaneous reperfusion that characterizes Wellens' Syndrome (See ECG Blog #350).
  • While Wellens' Syndrome most often involves a high-grade proximal LAD (Left Anterior Descending) stenosis that results in anterior reperfusion T waves — the same pathophysiology of Wellens' Syndrome may also be seen in the form of infero-postero reperfusion waves from recent RCA or LCx occlusion (See ECG Blog #326).

  • PEARL #4: The importance of recognizing the correlation between ECG findings and the history in today's case (ie, a prior history of chest pain that has resolved at the time the reperfusion T waves in ECG #1 are seen) — suggests the need for timely cath, with expected need for PCI pending cath findings (to prevent reocclusion of the "culprit" artery that spontaneously reopened).

  • How likely is it that toda's patient may have had Mobitz I 2nd-degree AV block earlier in the week?

It is common for patient's with acute inferior MI — to develop a stepwise sequence of AV conduction disturbances, resulting from associated ischemia in the AV node.
  • Conduction disturbances in such patients tend to begin with the simple PR interval prolongation of 1st-degree AV block — followed by progression to 2nd-degree AV block of the Mobitz I type (ie, AV Wenckebach). Some patients ultimately progress to 3rd-degree (ie, complete) AV block, most often with a narrow (AV nodal) escape rhythm. 
  • In most cases in which AV conduction disturbances develop with acute inferior MI — the progression is sequential (ie, from 1st-degree — to 2nd-degree — to 3rd-degree). Conduction disturbances in such patients tend to be transient — with regression in the reverse sequence over the ensuing period of days to 1-2 weeks, as the patient recovers from their infarction.

  • BOTTOM Line: The fact that today's patient had a recent inferior MI — and now presents with marked PR interval prolongation — could be perfectly consistent with having had a recent Mobitz I block, that is now in process of resolving as the patient recovers from her infarction.

  • PEARL #5: Most patients with 1st-degree AV block remain asymptomatic without the need for intervention. This is especially true when the severity of 1st-degree AV block is not great (ie, a PR interval less than 0.30 second)Once the PR interval extends beyond 0.30 second (as is the case in today's patient) — the delay in ventricular contraction that occurs may result in the atria contracting against closed AV valves, with reduction in cardiac output. This may lead to a series of symptoms similar to “pacemaker syndrome” (ie, dizziness, fatigue, light-headedness, presyncope/syncope, dyspnea and/or chest pain).
  • On occasion — symptoms in patients with a markedly prolonged PR interval may be severe enough to require implantation of a permanent pacemaker.

Comparison with the Prior ECG:
A previous (baseline) ECG on today's patient was found. For clarity in Figure-2 — I have put this prior ECG (obtained ~3 years earlier — when the patient was asymptomatic) — together with today's initial ECG.

  • Does comparison of the 2 tracings in Figure-2 support our theory regarding the likely sequence of events in today's case?

Figure-2: Comparison of today's tracing — with a baseline ECG from ~3 years earlier. Does this baseline tracing support our theory?

Comparison of the 2 ECGs in Figure-2:
Interpretation of today's initial ECG, in light of the baseline tracing from ~3 years earlier — is insightful. Note the absence of the following findings from ECG #2:
  • In the inferior leads of ECG #2 — there was no ST elevation or T wave inversion in this baseline tracing.
  • In the high-lateral leads (ie, leads I, aVL) — there was no ST depression with terminal T wave positivity.
  • In the anterior chest leads — the ST segments were gently upsloping (as they are supposed to be) in leads V2,V3,V4 — and the T waves in leads V1-thru-V4 were neither tall nor peaked.
  • There was no lateral chest lead ST depression (in V4,V5,V6) — and there was no T wave "imbalance" (ie, There was no positive T wave taller in lead V1 than in lead V6).
  • R wave progression in the baseline tracing was more natural (ie, Instead of abrupt transition to a predominantly positive QRS by lead V3 — transition to predominant positivity in the chest leads occurred more gradually in ECG #2).

  • Did YOU notice that 1st-degree AV block was present in the baseline ECG? (albeit to a significantly lesser degree = 0.26 second).

CASE Conclusion:
Although I lack specific follow-up to today's case — a number of closing comments can be made.
  • The clinical scenario in today's case differs from the more common scenario seen in the ED (Emergency Department) — or in the field by EMS personnel — in that instead of the patient presenting at the time of acute symptoms — the patient presents for care a number of days after their acute chest pain episode. (This is much more consistent with what I used to see as a Primary Care Attending in our Family Medicine Center, where I worked for 30 years.)
  • Patients with severe acute chest pain symptoms tend to "self-select" — either calling EMS directly, or getting to the ED by themself or with family. Since the majority of patients who die from acute MI, do so within the first 24-48 hours after onset — it is insightful to appreciate that the patient who only presents a few days after their symptoms, has probably already survived their "highest risk" period.

  • Given the history in today's case (interpreted in context with the 2 ECGs shown in Figure-2) — We have confirmed that all ST-T wave findings described above for ECG #1 were new since the baseline tracing. This supports our theory that the initial ECG in today's case represents reperfusion following a recent OMI that occurred days earlier. Consistent with Wellens' Syndrome — timely cath is still indicated to clarify the anatomy, albeit the "culprit" artery is most probably open at this time since the patient remains pain-free.

  • On the other hand — the 1st-degree AV block is not new! — since the PR interval was ~0.26 second on the baseline tracing done ~3 years ago. As a result (unless additional baseline tracings are available) — we really do not know if this patient had been progressively increasing the severity of her 1st-degree AV block over a period of years — or — if her conduction defect had been stable with a PR interval ~0.26 second for the past 3 years, only to increase this past week at the time of her acute OMI. The answer to this question may have implications regarding the potential need for permanent pacing in this older woman (ie, As noted above — it's possible if her severe 1st-degree AV block persists or worsens — that permanent pacing may eventually be needed).


Acknowledgment: My appreciation to Arron Pearce (from Manchester, UK) 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 #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 (as well as reviewing why the term "STEMI" — should replaced by "OMI" = Occlusion-based MI).

  • ECG Blog #285 — and ECG Blog #246 — and ECG Blog #80 — for examples of acute posterior MI (with use of the Mirror Test to facilitate diagnosis).
  • ECG Blog #317 — reviews use (or not) of Posterior Leads.

  • ECG Blog #184 — and ECG Blog #167 — review the "magical" mirror-image opposite relationship between lead III and lead aVL that helps to confirm acute OMI.
  • The February 16, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) emphasizes utility of the Mirror Test for diagnosis of acute Posterior MI. 
  • Diagnosis of an OMI from the initial ECG — Serial tracings with spontaneous reperfusion — then reocclusion! — See My Comment at the bottom of the page in the October 14, 2020 post on Dr. Smith's ECG Blog.
  • Acute OMI that wasn’t accepted by the Attending — See My Comment at the bottom of the page in the November 21, 2020 post on Dr. Smith’s ECG Blog.
  • Another overlooked OMI (Cardiologist limited by STEMI Definition — OMI evident by Mirror Test) — See My Comment at the bottom of the page in the September 21, 2020 post on Dr. Smith’s ECG Blog.
  • Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.

  • ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.

  • ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
  • ECG Blog #230 — Reviews how to compare Serial ECGs.
  • ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
  • ECG Blog #268 — Shows an example of reperfusion T waves.

  • ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).
  • ECG Blog #350 — Reviews another case of Wellens' Syndrome (with T wave "imbalance" in the chest leads between leads V1,V6).

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