This 12-lead ECG was
obtained from a 61-year old man who was seen by EMS for new-onset chest
discomfort. How would you interpret this ECG? Should you call to activate the cath lab en route to the
hospital?
Figure-1: 12-lead ECG obtained from a 61-year old man with new-onset chest discomfort. Would you activate the cath lab for suspected acute anterior STEMI? |
Interpretation: There are a number of
findings on this ECG that make it difficult not
to immediately activate the cath lab. We note the following:
The rhythm is sinus.
Intervals are normal. The axis is slightly leftward (at about -15 degrees). Voltage for LVH is satisfied by an R wave in lead aVL that clearly exceeds 12mm
in amplitude.
- There is a Q wave in lead V1, a QS in V2 — and no more than the tiniest of r waves in lead V3. Thus, R wave amplitude is clearly reduced in the anterior leads — and Q waves in V1,V2 could be consistent with septal infarction.
- The T wave in leads V2-thru-V5 looks like it may be hyperacute. T wave amplitude in lead V2 seems disproportionately tall compared to the QRS complex in this lead. In addition, the amount of J-point elevation in leads V4 and V5 seems more-than-is-normally-expected in these leads, especially given relatively small R waves in V4,V5.
- There is ST elevation in lead aVL that looks to be the mirror-image of lead III.
- There appears to be reciprocal change in the inferior leads (more subtle in lead II, since there is only some ST-T flattening in this lead …).
Considering the above
findings together — one needs to be concerned about the possibility of
acute LAD occlusion in this 61-year old man with new-onset symptoms. That said,
there are a number of features against
this being an acute anterior STEMI. These include:
- Probable Lead Malposition — It is surprising how frequently leads V1 and V2 are placed too high on the chest. Doing so may give false impression of anterior infarction. Clues that precordial leads have probably been placed one (or even two) interspaces too high include: i) a significant negative component to the P wave in lead V1 and/or V2; and, ii) the finding of an r’ deflection in either V1 and/or V2. Both of these findings are present in Figure-1. Perhaps lead V3 is then also malpositioned? So maybe there is not loss of r wave (and development of Q waves) after all in the anterior leads?
- The mean QRS Axis is Leftward. This might account for normal T wave inversion in predominantly negative limb leads III and aVF.
- Early Repolarization in Leads I, aVL? — Shape of the J-point ST elevation in these lateral leads is concave-up (ie, “smiley”-configuration) with small, narrow septal q waves and J-point notching. This has the appearance of early repolarization.
- There is LVH. As mentioned, voltage criteria for LVH are clearly met in lead aVL (that easily surpasses an R wave amplitude of ≥12mm). What about R wave amplitude in lead V6? Close vertical placement of lateral chest leads with resultant overlap makes it very difficult to discern just how tall the R wave in lead V6 is, but I suspect it surpasses 18mm once one mentally “subtracts” the overlap. LVH is notorious for producing a reciprocal “strain” pattern in anterior leads — and this could account for at least some of the suspicious T wave appearance in leads V2,V3.
BOTTOM LINE — If the history in this case was worrisome,
then this patient most likely needs timely cardiac catheterization. One has to
be able to rule out acute stemi with more
certainty than I have from looking at this single tracing. But my thought on
seeing this ECG was that I would not
be surprised if cath turned out to be unremarkable.
- That said, there DOES seem to be more ST elevation-than-I-would-expect given QRS appearance in leads V4,V5 — so I would also not be surprised if cath showed acute LAD occlusion.
- It is FINE not to be certain from review of a single tracing as to whether or not acute infarction is occurring. Depending on clinical circumstances — one might either decide to repeat the ECG and obtain stat Echo (looking for wall motion abnormality) in the Emergency Department — or, simply proceed to cath for definitive diagnosis.
- Follow-Up — This patient did not have acute infarction ...
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Acknowledgment: — My thanks to Dustin
Carter and James Criscitiello (from New
York, New York) for their permission to use this case and ECG.
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Why do they malposition these leads???
ReplyDeleteLead malposition is of course not "intentional" — but I suspect folks are either in a hurry (such that they do not carefully assess landmarks) — or perhaps they were taught by others who just didn't think precise attention to anatomic landmarks was important. This is a nice short article on the subject — https://www.dropbox.com/s/0uruf8w81j1o5j7/Precordial%20lead%20misplace-Javier%20Garcia-Niebla.pdf?dl=0 —
DeleteGreat case. Good learning points. Thnx Prof.
ReplyDeleteThanks for the kind words — :)
DeleteAnother great case.... Thank you
ReplyDelete