Saturday, June 29, 2019

ECG Blog #165 (MI - Acute - Old - Unknown Age - Aneurysm - Fragmentation)

Imagine you are overreading tracings that were done in an ED (Emergency Department). Unfortunately, you have NO clinical information on the patient whose ECG is shown in Figure-1.
  • How would you interpret this ECG?
  • Clinically — What do you suspect is going on with this patient?
Figure-1: 12-Lead ECG obtained from a patient who presented to the ED. Unfortunately — NO clinical information is available. How do you interpret this tracing? (See text). NOTE — Enlarge by clicking on the Figure.

Descriptive Analysis of the ECG in Figure-1:
An upright P wave with a normal PR interval is seen in lead II. The ventricular rhythm is fairly regular — and the QRS complex is not widened (ie, not more than 0.10 second) — therefore, this is a sinus rhythm at ~60-65/minute.
  • All intervals are normal (ie, the PR interval is not more than 1 large box in duration — the QRS not more than 1/2 a large box — and the QT not more than 1/2 the R-R interval).
  • There is a markedly leftward axis (ie, the QRS is predominantly positive in lead I — but all negative in lead aVF).
  • There is no chamber enlargement.
The main abnormalities are in assessment of Q-R-S-Changes:
  • Q Waves — Small and narrow q waves are seen in leads I and aVL. Entirely negative QS complexes are seen in leads II, aVF; and V2, V3. Larger and/or wider-than-expected Q waves are seen in leads V4, V5 and V6.
  • R Wave Progression — Transition is slightly delayed, since the R wave does not become taller than the S wave is deep until between leads V4-to-V5. NOTE: There is an initial positive deflection (r wave) in lead V1. This small initial r wave is then lost as the fragmented and entirely negative QS complex in lead V2 forms (ie, there is Loss oR Wave” as we move from lead V1-to-V2).
  • ST-T Wave Changes — There is nonspecific ST-T wave flattening in lead aVL. There is straightening of the ST segment takeoff in several anterior leads (slanted BLUE lines in Figure-2). Slight ST elevation is seen in lead V1 — and then 2-3 mm of J-point Selevation is seen in leads V2V3 and V4 (small PURPLE arrows above the dotted RED line baseline).
  • Other Findings — There is fragmentation of the QRS that deforms the downslope of the S wave in a number of leads (small BLUE arrows).
Figure-2: We’ve labeled Figure-1. Small BLUE arrows highlight fragmentationSlanted BLUE lines indicate straightening of the ST segment takeoff in several leads. The dotted RED lines with small PURPLE arrows indicate the amount of ST elevation in several anterior leads (See text).

Clinical Impression /Clinical Notes: As stated — We were not provided with any clinical information, other than that this patient presented to the ED.
  • The rhythm is sinus at ~60-65/minute.
  • Marked left axis deviation is present. It is difficult to determine if the reason for this is: iLAHB (Left Anterior Hemi-Block)iiInferior MI of uncertain age; and/oriiiBoth LAHB prior Inferior MI.
  • Identification of fragmentation (ie, irregularitiesin one or more QRS complexes (small BLUE arrows) suggests scarring — that may be the result of prior infarction, cardiomyopathy, or some other form of structural heart disease. Such fragmentation does not tell us whether heart disease is acute or has been present long-term — but it nonetheless is an invaluable clue for conveying that the patient in question almost certainly has some form of underlying structural heart disease.
  • Returning to assessment of the inferior leads — the finding of fragmentation (irregularityof S wave downslope in lead aVF — and especially the QRS shape in lead II (which suggests an initial Q wave, that is aborted by a small positive deflection that fails to reach to baseline, before continuing on as a deep S wave— strongly suggests that there has been inferior MI at somepoint in time. Lack of any inferior lead ST elevation the nonspecific ST-T wave flattening in lead aVL suggest this to be an old inferior MI.
  • Finally — the small, thin initial r wave in lead III is against inferior MI, and strongly suggests LAHB.
  • My Take” — Inferior MI and LAHB are competing” conditions — in that the presence of one may mask the other. Given the conflicting ECG findings described above — I strongly suspect that there is both LAHB old inferior MI.
Assessment of Chest Leads in Figure-2: We can say with some certainty that extensive Anterior Mhas occurred at some point in time because: iAs noted above — there is Loss of Wave in going from lead V1-to-V2; iiDeep QS complexes are seen in leads V2 and V3; andiiiDeep Q waves continue in leads V4 and V5 — and the Q wave in lead V6 is wider-than-expected for a “septal” Q wave.
  • Preservation of the initial r wave in lead V1 suggests (at least in theory) — that the septum remains intact (it is the initial left-to-right vector of septal depolarization that produces the initial r wave in lead V1; This is lost with septal infarction). We would therefore describe the location of the MI in Figure-2 as “anterior” or “antero-lateral” — but not “antero-septal” (because the initial r wave in lead V1 is preserved).
In contrast to the picture in the inferior leads (in which we see Q waves in leads II and aVF — but no ST elevation) — there is significant ST elevation that begins in lead V1, and attains 2-3 mm in leads V2-thru-V4. This raises the QUESTION of whether the Anterior Min Figure-2 is: inew or recent?; iiold?or perhapsiiian “old” MI with superimposed new or recent injury?
  • Finding a prior ECG on this patient could be of invaluable assistance in answering this question — since this will tell you which of the above ECG findings were previously present. But without a prior ECG — it is virtually impossible to be certain ...
  • The History is extremely important! We were told that the ECG in Figure-2 was recorded in the ED — but we were not told if the patient was asymptomatic or having new-onset chest pain at the time ... IF the history for this patient did not sound like an acute MI — this would support the likelihood that the changes were not new.
  • Repeating the ECG in the ED a little while later may help. An acute evolving STEMI tends to show evolution of ECG changes, sometimes over a surprisingly short period of time.
  • Doing an Echo in the ED may help! Seeing a large LV (left ventricularaneurysm with reduced or absent contractility would support chronicity rather than acute MI.
MHUNCH: I believe it most likely that extensive antero-lateral MI occurred in the past for the ECG shown in Figure-2 because: iThere is a lot of fragmentation (this usually though not always takes time to develop); iiConsidering that QS complexes and/or large Q waves occur in 5 of the 6 chest leads — the amount of ST elevation is relatively modest; andiiiThe ST segment takeoff in anterior leads shows straightening (slanted BLUE lines in Figure-2) — but lacks the coved ST segment appearance that is more characteristic of acute injury.
  • BOTTOM Line: Clinical correlation will be needed to arrive at a definitive answer (ie, history; finding a prior tracing; serum troponin values, Echo, serial ECGs in the ED, etc.). That said — the KEY Points from this blog post are: iTo recognize ECG findings suggestive of new or recent vs old infarction; iiTo realize that you may not be able to “date” the infarction on the basis of a single ECG without clinical correlation; andiiiTo appreciate that the ECG picture seen in Figure-2 would be perfectly consistent with development of LAneurysm following extensive Anterior MI.




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