Wednesday, May 26, 2021

ECG Blog #228 — What is the Main Problem?

The 12-lead ECG and long lead II rhythm strip shown in Figure-1 was obtained from a middle-aged woman with a several day history of fever and shortness of breath. She had palpitations — but NO chest pain. The patient tested positive for Covid-19 several days earlier.

  • How would YOU interpret this tracing?
  •   What is the main problem? 


Figure-1: ECG obtained from a middle-aged woman with fever, dyspnea, palpitations, and a positive test for Covid-19. NO chest pain.



NOTE #1: Some readers may prefer at this point to listen to the 3:30 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-44).


Today’s ECG Media PEARL #44 (3:30 minutes Audio) — What is a "Silent" MI? — and How OFTEN do "Silent MIs" occur? (results from Framingham — 5/24/2021).



MY Initial Approach to the ECG in Figure-1:

Unfortunately, the tracing in Figure-1 is curved — therefore a bit distorted (was sent to me via the internet). That said — this ECG is of good enough quality to appreciate the important ECG findings.

  • The rhythm is venricular bigeminy — that is, every-other-beat ( = beats #1, 3, 5, 7, 9, 11, 13 and 15) is a PVC (Premature Ventricular Contraction). We know these beats are PVCs — because the QRS complex is wide; it looks very different than the sinus-conducted beats; and the QRS of these wide beats is not preceded by a P wave.

PEARL #1: To determine what else might be ongoing in this ECG — We need to focus on ST-T wave morphology of sinus-conducted beats in all 12-leads (ie, for beats #2, 4, 6, 8, 10, 12 and 14)

  • Beyond-the-Core: There are 2 possible exceptions to the statement I just made, namely that, "We need to focus on ST-T wave morphology of sinus-conducted beats". It is uncommon that either of these exceptions will apply — but for advanced interpreters, it is worthwhile being aware of them: i) Ventricular ectopy itself (not necessarily related to acute or longterm coronary disease) may alter the ST-T wave of the sinus-conducted beat that follows a PVC; andii) On occasion, it is the ST-T wave of a PVC that provides the best indication of acute coronary disease (ie, when the PVC shows obviously abnormal ST elevation or depression).



Because of the large size and frequency of the PVCs in Figure-1 — it might be EASY to overlook the abnormal ST-T wave findings of the sinus-conducted beats. 

  • To facilitate this assessment — I have enclosed the QRS complex and ST-T wave of each of the sinus-conducted beats in all 12 leads within a BLUE-WHITE rectangle (Figure-2).



Figure-2: I've enclosed the QRS complex and ST-T wave from all sinus-conducted beats within one of the BLUE-WHITE rectangles (See text).


MY Interpretation of Figure-2:

QRS amplitude for each of the 6 limb leads is small, especially in comparison to the much larger amplitude of the PVCs.

  • There is ST segment coving and slight-but-real ST elevation in each of the 3 inferior leads (II, III, aVF). ST elevation is most marked in lead III — and the "takeoff" of the ST segment in all 3 inferior leads is abnormally straightened (slanted BLUE lines drawn parallel to the ST segment "takeoff" in these 3 leads).
  • Confirmation of recent or acute inferior infarction is forthcoming from the finding of reciprocal ST depressionin high-lateral leads I and aVL.
  • Associated posterior MI is diagnosed by: i) Early transition, with a predominantly positive R wave already in lead V2; andii) Shelf-like ST depression in the anterior leads, that is maximal in lead V3.
  • There is also ST-T wave flattening with slight depression in the lateral chest leads (V4, V5 and V6).


Putting It All Together:

This middle-aged woman with fever, dyspnea with Covid-19 positivity and palpitations — but no chest pain— presented to the ED with a very abnormal ECG:

  • The rhythm was ventricular bigeminy.
  • Assessment of QRST morphology of sinus-conducted beats (Figure-2) — suggested recent (if not acute) infero-postero MI.
  • The reason for the frequent PVCs is most probably the recent acute MI.
  • PEARL #2: This patient had a number of acute symptoms — but no chest pain. This satisfies the definition of a "silent" MI (which is the topic of our brief Audio Pearl #44See above!)

The Case Continued:

A follow-up ECG was obtained on this patient (Figure-3). Now that the PVCs have resolved in ECG #2 — Isn't it easier to identify the acute findings on this tracing!

  • QUESTION: What is the probable "culprit" artery?



Figure-3: Follow-up ECG obtained in today's case (See text).




The rhythm in ECG #2 (shown in Figure-3) is sinus at ~75/minute. All intervals are normal. There is slight axis deviation — but not enough to qualify as LAHB (ie, the QRS is still predominantly positive in lead II). There is no chamber enlargement.

  • A large Q wave is now seen in lead III (A small-but-present initial r wave was seen in lead III in Figure-2).
  • R wave progression in Figure-3 is abnormal — with early transition and a predominant R wave already in lead V2.
  • Although QRS amplitude in the limb leads remains small — there appears to be more ST elevation in inferior leads III and aVF than there had been in Figure-2.
  • The ST depression in lead aVL is also increased compared to Figure-2 — and now takes on a "magical" mirror-image opposite picture, compared to the shape of the ST elevation in lead III (See ECG Blog #184 for more on this "magical" mirror-image opposite picture between leads III and aVL in the setting of acute infarction).
  • In the chest leads — We have already noted the early transition with a surprisingly tall R wave already in lead V2. This is associated with marked ST depression in lead V2, with terminal positivity of the T wave. The ECG appearance of the QRST complex in lead V2 constitutes a positive "Mirror Test" — that is virtually diagnostic of acute posterior MI (See ECG Blog #80 and ECG Blog #56). But what is most remarkable about the ST-T waves in the chest leads of Figure-3 — is that despite marked ST depression in lead V2, there is virtually no ST depression in lead V1. This suggests the strong possibility of associated acute RV (Right Ventricular) infarction (See ECG Blog #190-LINK).
  • PEARL #3: The probable "culprit" artery in today's case is the RCA (Right Coronary Artery) because: iAcute infero-postero MI in the absence of anterior ST elevation narrows down the possibilities for the "culprit" artery to the RCA or the LCx (Left Circumflex) coronary artery — and 80-90% of individuals have a right-dominant circulation (ie, statistical odds favor the RCA); ii) The finding of more ST elevation in lead III > II — together with marked, mirror-image opposite reciprocal ST depression in lead aVL favors the RCA; andiiiThe flat ST segment in lead V1, in association with marked ST depression in lead V2 suggests acute RV involvement — and the LCx does not vascularize the right ventricle.


Case Follow-Up:

The acute MI was recognized by the treating clinicians. Since acute cath facilities were not available — the patient was treated with thrombolytic therapy.



Acknowledgment: My appreciation to Drs. Chamanti and Anil Kumar Kolli (from Indiafor the case and this tracing.



Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #184 — Reviews the "Magical" Lead 3-Lead aVL Relationship with acute OMI (Occlusion-based Myocardial Infarction). 
  • ECG Blog #80 — Reviews the positive "Mirror Test" for ECG diagnosis of acute posterior MI — as well as the basics for predicting the "culprit" artery with acute MI. 
  • ECG Blog #56 — Reviews the positive "Mirror Test" for ECG diagnosis of acute posterior MI
  • ECG Blog #190 — Reviews the ECG diagnosis of acute RV (Right Ventricular) MI
  • ECG Blog #193 — Reviews the concept of "OMI" ( = Occlusion-based Myocardial Infarction) — with some basics on the "Mirror Test" — and for predicting the "culprit" artery plus links to PDF summaries and numerous other acute MI cases from my ECG Blog.

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