Saturday, December 8, 2012

ECG Blog #56 — A Mirror-Image View

You are asked to interpret the ECG in Figure 1. You are told that the patient was just resuscitated from cardiac arrest. This is his post-resuscitation 12-lead ECG.
  • In light of this history – How would you interpret this ECG?
  • Given that the patient was just resuscitated – What treatment would you recommend?
  • What would you expect to see on cath?

Figure 1: 12-lead ECG obtained immediately post-resuscitation. What would you expect to find on cath? 

INTERPRETATION: There is sinus rhythm at a rate ~85/minute (upright P wave with fixed PR interval in lead II). All intervals (PR/QRS/QT) and the axis are normal. No chamber enlargement. Regarding Q‑R‑S‑T Changes:
  • There is a narrow but deep Q wave in lead III – but no other Q waves.
  • An rSr’ complex is seen in lead V1.
  • Transition occurs early with a relatively tall R wave already by lead V2.
  • ST segments show significant coved ST elevation in each inferior lead (II,III,aVF) – as well as in lateral precordial leads V5,V6. ST depression is seen in leads I, aVL and V2.
  • Beyond-the-Core: There may be slight ST elevation in lead V1. There appears to be a peculiar downslope to the ST segment in lead V1 that blends into shallow T wave inversion in this lead.
IMPRESSION: The picture is consistent with acute infero-latero-postero STEMI (ST Elevation Myocardial Infarction) from acute RCA (Right Coronary Artery) occlusion. There may also be RV (Right Ventricular) involvement. Immediate cardiac catheterization is indicated in this post-resuscitation patient who may have arrested because of acute RCA occlusion that hopefully will be amenable to acute PCI (PerCutaneous Intervention). We emphasize the following points:
  • Acute inferior MI – is suggested by ST elevation in each of the inferior leads. ST segments have a “hyperacute” appearance – with broadening of the peak of the T wave in lead aVF; ST segment flattening in lead III – and straightening of the ascending limb of the ST segment in lead II. Taken together – this picture is highly suggestive of an acute inferior infarction.
  • Support that the inferior MI is acute is forthcoming from the presence of reciprocal ST depression (seen best in leads I, aVL and V2 ).
  • ST segment elevation in lead III is clearly more than in lead II. This finding is typically seen when there is acute RCA occlusion. Support of acute RCA occlusion is forthcoming from the marked ST depression seen in reciprocal lead aVL.
  • The RCA typically supplies the right ventricle – as well as the inferior and posterior walls of the left ventricle. As a result – one may see any combination of infero-, postero-, and/or right ventricular infarction when there is acute RCA occlusion. Clinically – one should always be on the “lookout” for evidence of RV (Right Ventricular) and posterior infarction whenever you see acute inferior ST elevation.
  • Acute Posterior MI is suggested in Figure 1 by: i) Early transition (producing sudden appearance of a predominant R wave by lead V2); ii) PositiveMirror Test”, especially in lead V2 (See Figure 2); and iii) the findings noted in i) and ii) occurring in the setting of acute inferior infarction.

Figure 2: Flipping the ECG in Figure 1 upside-down produces a mirror image of the electrocardiogram. The anterior leads (V1,V2,V3) now provide an ECG picture of what is occurring in the “mirror-image” posterior wall. The positive Mirror Test” is best seen in flipped-over lead V2 in this example – which now manifests a deep Q, ST elevation and T wave inversion suggestive of acute posterior MI (red arrows).
  • Acute RV MI – may also be occurring. Definitive diagnosis of acute RV MI requires right-sided leads, which should show progressively increasing ST elevation as one moves across the right precordium (usually peaking by lead V3R to V4R). Lacking right-sided leads in this case – We can only surmise the possibility of acute associated RV infarction based on: i) the finding of acute infero-postero MI with likely acute RCA occlusion; and ii) subtle presence of ST elevation in lead V1 of Figure 1 – but not in V2,V3 (whereas with anterior MI from acute LAD [Left Anterior Descending] occlusion there is usually ST elevation in at least several anterior leads).
  • Lateral Precordial ST Elevation – is also present in Figure 1. That is – there is subtle but real ST segment coving in both leads V4 and V5, with slight elevation of the J point in lead V5. The ST segment is more elevated in lead V6, and takes on a hyperacute appearance in this last lateral precordial lead. That said – it is not certain that ST elevation in V5,V6 represents acute “lateral” infarction – since this could also be a reciprocal change resulting from acute posterior infarction (lead V6 almost being situated anatomically opposite to anterior precordial leads).
  • The finding of acute infero-postero-lateral MI should make one consider the less common (~10-15%) anatomic variant of a left-dominant circulation – in which the circumflex artery is larger-than-usual, and extends to supply the inferior and posterior walls of the left ventricle. The RCA is a relatively smaller vessel in patients with left-dominant circulation. However, despite awareness of this anatomic variant – We still suspect the “culprit artery” in this case to be a proximal RCA (rather than left circumflex) occlusion given: i) marked ST segment elevation in lead III > lead II; ii) significant reciprocal ST depression (rather than ST elevation) in lead aVL; and iii) suspected RV involvement (suggested by the finding of ST elevation in lead V1 but not in V2,V3 in the setting of incomplete RBBB).
  • Beyond-the-Core: As noted in our Descriptive Analysis (above under Interpretation) – there is a peculiar downslope to the ST segment in lead V1 that blends into shallow T wave inversion in this lead. This appearance at least superficially resembles Brugada syndrome (See ECG Blog #50). Criteria for true Brugada syndrome are not met – because there is not at least 2mm of ST elevation with this downsloping ST segment shape in at least 2 anterior precordial leads. Nevertheless, since this patient is manifesting an acute STEMI and was just resuscitated – the ST-T wave appearance in lead V1 is at least worthy of follow-up (Click HERE for more on Brugada Syndrome).
CONCLUSION: Unfortunately we do not have cath follow-up on this case – so our suspicion of acute RCA occlusion is unconfirmed as the “culprit artery”. That said, regardless of what the culprit artery might be – acute cath is indicated in this post-resuscitation patient who clearly manifests an acute STEMI that hopefully was treated with timely reperfusion.

Link to Section 10.0 for pdf download on the ECG Diagnosis of Acute MI (from our ECG-2014-ePub).
  • ECG Changes of Acute MI – begins in Section 10.1 - 
  • Discussion of the Coronary Circulation (and determining the "culprit" artery) – begins in Section 10.16 - 
  • Mirror Test (Posterior MI– begins in Section 10.33 -


  1. your blog helpful for me. your blog is very nice for me please keep it up.I like it
    Visit :- depression test

    1. THANK YOU Anderson for your kind reply. Please be sure to check out my ECG Videos ( — :)

  2. Thank you for your significant case and ecg presentation.

  3. Dr Dr Grauer,

    I have one question regarding the passage: "That said – it is not certain that ST elevation in V5,V6 represents acute “lateral” infarction – since this could also be a reciprocal change resulting from acute posterior infarction (lead V6 almost being situated anatomically opposite to anterior precordial leads).

    In my opinion ST-Elevation in V5/V6 can NOT be a reciprocal change of depression in V1/V2 because elevation is where the ischemia is. So Elevation in V5/V6 indicates Ischemia in the lateral segment. The depression in V1/V2 is indictating ischemia in the posterioer segement.

    Do you agreee?

    Thank you,

    1. Thank you for your comment. First — I’ll mention that I wrote this post in 2012, or 9 years ago … As to this case — the major area of ST elevation is in the inferior leads which is most likely from acute RCA occlusion.

      I’ll discount the ST-T wave in lead V1 — because the shape of this ST elevation in lead V1 looks most like Brugada phenocopy (although the amount of ST elevation is less than is usually seen with Brugada phenocopy, probably because some of the ST elevation is being cancelled out by what would have been ST depression.

      Rather than “ischemia” of the posterior segment — I interpret the shape & amount of ST depression that we see in lead V2 (given that we KNOW there is acute inferior lead ST elevation) — so the ST depression in lead V2 by my terminology is a “stemi-equivalent” (ie, there is a positive “Mirror Test” — since this anterior lead V2 gives us a “mirror-image” view of what is going on in the posterior wall).

      As to the ST elevation that we see in lateral chest leads (most marked in lead V6) — we enter into semantics. As an isolated lesion — we’d think about LCx (Left CircumfleX) involvement … — but as part of the main lesion in today’s case ( = arising from presumed acute RCA occlusion), you sometimes see ST elevation in lateral chest leads when there is involvement of prominent posterior-lateral branches of the PDA (Posterior Descending Artery). Is this “lateral” — or is this “posterior”? With acute posterior involvement, we tend to see the ST elevation in “more lateral” (ergo posterior) leads V7, V8, V9 — and perhaps what we are seeing in today’s case is that ST elevation in lead V6 is on its way to even more ST elevation in V7,8,9?

      I agree you could question my choice of the word “reciprocal” here — but the concept I meant to convey is that the ST depression in lead V2 is the result of a “stemi-equivalent” for acute posterior infarction — and since lead V6 is almost “opposite” anatomically to lead V2 — we might as a result see ST elevation there.

      BOTTOM LINE (beyond semantics) — There is clear evidence of acute OMI ( = Occlusion-based MI) following cardiac arrest in this patient — with it being academic as to where … since prompt cath is clearly indicated regardless. I have no trouble simply interpreting this tracing as showing acute infero-postero-lateral MI due to acute coronary occusion.

      THANKS again for your comment! — :)